1. Innate Immune Response Speed
Why is the innate immune response faster than the adaptive immune response?
A: Because it involves the production of specific antibodies
B: Because it requires activation by antigen-presenting cells
C: Because it relies on pre-existing cells and mechanisms that are always active
D: Because it involves memory cells that respond quickly
Answer: C: Because it relies on pre-existing cells and mechanisms that are always active
2. Role of Macrophages in Innate Immunity
How do macrophages contribute to innate immunity?
A: By producing specific antibodies against pathogens
B: By phagocytosing pathogens and presenting antigens to adaptive immune cells
C: By secreting cytokines that activate B cells
D: By producing memory cells that respond to future infections
Answer: B: By phagocytosing pathogens and presenting antigens to adaptive immune cells
3. Antigen Recognition by T-Cells
How do T-cells in adaptive immunity recognize antigens?
A: By binding to peptides presented on MHC molecules of antigen-presenting cells
B: By directly binding to pathogens without needing antigen presentation
C: By recognizing lipids and carbohydrates on pathogens
D: By secreting antibodies that neutralize pathogens
Answer: A: By binding to peptides presented on MHC molecules of antigen-presenting cells
4. Complement System and Innate Immunity
What is the role of the complement system in innate immunity?
A: To produce antibodies against pathogens
B: To activate memory cells in response to infection
C: To present antigens to T cells
D: To lyse pathogens directly or tag them for destruction by phagocytes
Answer: D: To lyse pathogens directly or tag them for destruction by phagocytes
5. Specificity of Adaptive Immunity
What is a hallmark feature of adaptive immunity compared to innate immunity?
A: It has antigen-specific responses, targeting particular pathogens
B: It provides a rapid, non-specific response to any pathogen
C: It relies on pre-formed antibodies in the bloodstream
D: It acts without the need for T or B cells
Answer: A: It has antigen-specific responses, targeting particular pathogens
6. Role of Natural Killer (NK) Cells
How do natural killer (NK) cells contribute to the innate immune response?
A: By producing antibodies against viral antigens
B: By activating the adaptive immune response through antigen presentation
C: By differentiating into memory cells after an infection
D: By directly killing virus-infected cells and tumor cells without prior sensitization
Answer: D: By directly killing virus-infected cells and tumor cells without prior sensitization
7. Helper T Cells and Adaptive Immunity
What is the primary role of helper T cells (CD4+) in adaptive immunity?
A: To phagocytose pathogens and debris
B: To activate B cells and cytotoxic T cells through cytokine secretion
C: To secrete antibodies against pathogens
D: To induce apoptosis in infected cells
Answer: B: To activate B cells and cytotoxic T cells through cytokine secretion
8. Innate Immunity's Role in Inflammation
How does the innate immune system trigger inflammation in response to infection?
A: By activating memory cells to produce cytokines
B: By activating complement proteins that attack pathogens
C: By releasing cytokines and chemokines that recruit immune cells to the infection site
D: By promoting the activation of B and T cells
Answer: C: By releasing cytokines and chemokines that recruit immune cells to the infection site
9. Immunological Memory
Which component of the immune system is responsible for immunological memory, providing a faster and stronger response upon subsequent exposure to the same pathogen?
A: Natural killer cells
B: Neutrophils
C: Dendritic cells
D: Memory B and T cells
Answer: D: Memory B and T cells
10. Pattern Recognition Receptors (PRRs)
What role do pattern recognition receptors (PRRs) play in the innate immune system?
A: They recognize conserved molecular patterns on pathogens, initiating an immune response
B: They differentiate between self and non-self antigens on pathogens
C: They produce specific antibodies against pathogens
D: They activate memory T cells to enhance future immune responses
Answer: A: They recognize conserved molecular patterns on pathogens, initiating an immune response
11. MHC Class I Antigen Processing Pathway
How are endogenous antigens processed and presented by MHC Class I molecules?
A: By direct binding to MHC Class I molecules on the cell surface
B: By being endocytosed and processed in lysosomes
C: By being degraded by the proteasome and presented to CD8+ T cells
D: By binding to MHC Class II molecules on antigen-presenting cells
Answer: C: By being degraded by the proteasome and presented to CD8+ T cells
12. Role of Dendritic Cells in Antigen Presentation
What is the primary role of dendritic cells in the immune response?
A: To secrete antibodies against specific pathogens
B: To capture antigens, process them, and present them to T cells
C: To destroy pathogens through phagocytosis
D: To inhibit the proliferation of T cells
Answer: B: To capture antigens, process them, and present them to T cells
13. MHC Class II and Exogenous Antigens
Which pathway is responsible for the presentation of exogenous antigens by MHC Class II molecules?
A: Antigen processing in the endosomal/lysosomal pathway
B: Direct presentation of antigens from the cytoplasm
C: Antigen degradation by the proteasome
D: Transfer of antigens to the Golgi apparatus
Answer: A: Antigen processing in the endosomal/lysosomal pathway
14. Cross-Presentation by Dendritic Cells
What is cross-presentation, and why is it important?
A: It is the presentation of self-antigens by MHC Class II molecules
B: It allows dendritic cells to present antigens to B cells
C: It refers to the transfer of antigens from one cell to another for presentation
D: It enables dendritic cells to present exogenous antigens via MHC Class I to CD8+ T cells
Answer: D: It enables dendritic cells to present exogenous antigens via MHC Class I to CD8+ T cells
15. Role of TAP Proteins in Antigen Presentation
What is the function of TAP (Transporter Associated with Antigen Processing) proteins in MHC Class I antigen presentation?
A: To transport peptides from the cytosol into the endoplasmic reticulum for loading onto MHC Class I molecules
B: To transfer antigens to MHC Class II molecules
C: To bind directly to T cell receptors
D: To degrade peptides into smaller fragments
Answer: A: To transport peptides from the cytosol into the endoplasmic reticulum for loading onto MHC Class I molecules
16. Invariant Chain and MHC Class II Presentation
What is the role of the invariant chain in MHC Class II antigen presentation?
A: To facilitate the binding of peptides to MHC Class I molecules
B: To enhance the affinity of MHC Class II for T cell receptors
C: To allow peptides to be processed in the cytoplasm
D: To prevent premature binding of peptides to MHC Class II molecules in the endoplasmic reticulum
Answer: D: To prevent premature binding of peptides to MHC Class II molecules in the endoplasmic reticulum
17. Co-Stimulation in T Cell Activation
What is the role of co-stimulation in T cell activation by dendritic cells?
A: It is unnecessary for T cell activation
B: It ensures full activation of T cells by providing a second signal in addition to antigen presentation
C: It blocks T cell receptors from binding to MHC molecules
D: It inhibits dendritic cell maturation
Answer: B: It ensures full activation of T cells by providing a second signal in addition to antigen presentation
18. MHC Polymorphism and Immune Response
How does the polymorphism of MHC genes affect the immune response?
A: It increases the likelihood of autoimmune diseases
B: It restricts the variety of antigens that can be presented by MHC molecules
C: It enhances the diversity of peptides that can be presented to T cells, improving immune recognition
D: It decreases the ability of dendritic cells to present antigens
Answer: C: It enhances the diversity of peptides that can be presented to T cells, improving immune recognition
19. CLIP Peptide in MHC Class II Processing
What is the function of the CLIP (Class II-associated Invariant Chain Peptide) in the MHC Class II processing pathway?
A: To assist in peptide binding to MHC Class I molecules
B: To degrade antigens for presentation
C: To transport MHC Class II molecules to the cell surface
D: To occupy the peptide-binding groove of MHC Class II until appropriate antigens are available
Answer: D: To occupy the peptide-binding groove of MHC Class II until appropriate antigens are available
20. T Cell Receptor Interaction with MHC-Peptide Complex
What is the primary interaction between a T cell receptor (TCR) and an antigen-presenting cell?
A: The TCR binds to the MHC-peptide complex on the surface of the antigen-presenting cell
B: The TCR binds to free antigens in the bloodstream
C: The TCR directly binds to the invariant chain
D: The TCR prevents the activation of other immune cells
Answer: A: The TCR binds to the MHC-peptide complex on the surface of the antigen-presenting cell
21. Activation of B Cells
What is the primary requirement for the activation of B cells during the immune response?
A: Direct contact with pathogen-associated molecular patterns
B: Antigen presentation by cytotoxic T cells
C: Binding of antigen to the B cell receptor (BCR) followed by co-stimulation
D: Release of interferons by infected cells
Answer: C: Binding of antigen to the B cell receptor (BCR) followed by co-stimulation
22. Role of Helper T Cells in B Cell Activation
How do helper T cells assist in the activation of B cells?
A: By directly producing antibodies
B: By providing co-stimulatory signals through CD40L-CD40 interactions
C: By releasing histamine to enhance the immune response
D: By inhibiting the activation of regulatory B cells
Answer: B: By providing co-stimulatory signals through CD40L-CD40 interactions
23. Primary Role of Plasma Cells
What is the main function of plasma cells in humoral immunity?
A: To secrete large amounts of antibodies specific to the activating antigen
B: To present antigens to helper T cells
C: To suppress the immune response during infection
D: To produce memory B cells
Answer: A: To secrete large amounts of antibodies specific to the activating antigen
24. Isotype Switching in B Cells
What determines the specific class (isotype) of antibodies produced by B cells during an immune response?
A: The type of pathogen that is encountered
B: The presence of memory T cells
C: The initial signal provided by antigen-presenting cells
D: Cytokines secreted by helper T cells during B cell activation
Answer: D: Cytokines secreted by helper T cells during B cell activation
25. Memory B Cells and Long-Term Immunity
How do memory B cells contribute to long-term immunity?
A: By rapidly differentiating into plasma cells upon re-exposure to the antigen
B: By constantly secreting low levels of antibodies
C: By preventing the activation of naive B cells
D: By enhancing the function of cytotoxic T cells
Answer: A: By rapidly differentiating into plasma cells upon re-exposure to the antigen
26. Germinal Centers in Lymphoid Tissue
What is the role of germinal centers in lymphoid tissue during a humoral immune response?
A: To trap pathogens and present them to cytotoxic T cells
B: To provide a site for macrophages to engulf antigens
C: To directly secrete antibodies into the bloodstream
D: To facilitate B cell proliferation, somatic hypermutation, and affinity maturation
Answer: D: To facilitate B cell proliferation, somatic hypermutation, and affinity maturation
27. Affinity Maturation and Antibody Specificity
How does affinity maturation enhance the effectiveness of antibodies?
A: By altering the antigen structure to make it more recognizable
B: By selecting for B cells with higher-affinity receptors for the antigen
C: By reducing the diversity of the B cell repertoire
D: By increasing the number of B cells that recognize self-antigens
Answer: B: By selecting for B cells with higher-affinity receptors for the antigen
28. Somatic Hypermutation in B Cells
What is the significance of somatic hypermutation in B cells during an immune response?
A: It increases the diversity of the antigen-binding region of antibodies
B: It promotes the release of cytokines that attract other immune cells
C: It leads to the production of antibodies with increased affinity for the antigen
D: It enhances the activation of dendritic cells
Answer: C: It leads to the production of antibodies with increased affinity for the antigen
29. Mechanism of Neutralization by Antibodies
How do antibodies neutralize pathogens during an infection?
A: By directly lysing the pathogen's cell membrane
B: By enhancing the release of inflammatory cytokines
C: By increasing the activity of cytotoxic T cells
D: By binding to the pathogen and preventing it from interacting with host cells
Answer: D: By binding to the pathogen and preventing it from interacting with host cells
30. Role of IgM in Primary Immune Response
Why is IgM typically the first antibody produced during a primary immune response?
A: Because it has a pentameric structure that allows for effective pathogen agglutination
B: Because it can cross the placental barrier
C: Because it is secreted by memory B cells
D: Because it has the highest affinity for antigens during an initial response
Answer: A: Because it has a pentameric structure that allows for effective pathogen agglutination
31. T Cell Receptor (TCR) Specificity
What determines the specificity of a T cell receptor (TCR) for its antigen?
A: The type of antigen-presenting cell that activates the T cell
B: The number of peptide antigens presented to the TCR
C: The unique combination of variable regions in the TCR's α and β chains
D: The presence of co-stimulatory molecules on the antigen-presenting cell
Answer: C: The unique combination of variable regions in the TCR's α and β chains
32. Role of CD28 in T Cell Activation
What is the function of CD28 in the activation of T cells?
A: It acts as a co-receptor for antigen recognition.
B: It provides a co-stimulatory signal necessary for full T cell activation.
C: It binds directly to the MHC-peptide complex on antigen-presenting cells.
D: It inhibits T cell activation to prevent autoimmunity.
Answer: B: It provides a co-stimulatory signal necessary for full T cell activation.
33. Th1 Cells and Cytokine Production
Which cytokine is primarily produced by Th1 cells and is critical for cell-mediated immunity?
A: Interferon-gamma (IFN-γ)
B: Interleukin-4 (IL-4)
C: Tumor necrosis factor-alpha (TNF-α)
D: Interleukin-10 (IL-10)
Answer: A: Interferon-gamma (IFN-γ)
34. Cytotoxic T Lymphocyte (CTL) Killing Mechanism
How do cytotoxic T lymphocytes (CTLs) induce apoptosis in infected target cells?
A: By producing high levels of cytokines
B: By inhibiting MHC class I presentation on infected cells
C: By phagocytosing infected cells
D: By releasing perforin and granzymes to trigger apoptosis
Answer: D: By releasing perforin and granzymes to trigger apoptosis
35. Antigen Presentation to CD8+ T Cells
What is required for antigen presentation to CD8+ cytotoxic T cells?
A: Peptides bound to MHC class I molecules on the surface of target cells
B: Antibodies bound to the surface of the pathogen
C: Peptides bound to MHC class II molecules on antigen-presenting cells
D: Direct binding of the pathogen to the T cell receptor
Answer: A: Peptides bound to MHC class I molecules on the surface of target cells
36. Regulatory T Cells and Immune Tolerance
How do regulatory T cells (Tregs) maintain immune tolerance?
A: By activating CTLs to eliminate self-reactive T cells
B: By enhancing the production of autoantibodies
C: By blocking co-stimulatory signals to effector T cells
D: By secreting immunosuppressive cytokines like IL-10 and TGF-β
Answer: D: By secreting immunosuppressive cytokines like IL-10 and TGF-β
37. Differentiation of Naive CD4+ T Cells
Which signal promotes the differentiation of naive CD4+ T cells into Th2 cells?
A: Interleukin-12 (IL-12)
B: Interleukin-4 (IL-4)
C: Tumor necrosis factor-alpha (TNF-α)
D: Interferon-gamma (IFN-γ)
Answer: B: Interleukin-4 (IL-4)
38. Role of T Cell Co-Stimulation in Autoimmunity
Why is the absence of co-stimulatory signals during antigen presentation critical in preventing autoimmunity?
A: It enhances T cell receptor binding to self-antigens.
B: It induces anergy in self-reactive T cells, preventing their activation.
C: It promotes the differentiation of effector T cells.
D: It increases the production of autoantibodies by B cells.
Answer: B: It induces anergy in self-reactive T cells, preventing their activation.
39. Th17 Cells and Inflammation
What is the primary role of Th17 cells in immune responses?
A: To promote antibody production
B: To inhibit inflammation by secreting IL-10
C: To enhance cytotoxic T cell responses
D: To mediate inflammatory responses, particularly against extracellular pathogens
Answer: D: To mediate inflammatory responses, particularly against extracellular pathogens
40. Memory T Cell Formation
How do memory T cells differ from naive T cells?
A: Memory T cells respond more rapidly upon re-exposure to their specific antigen.
B: Memory T cells require stronger co-stimulatory signals for activation.
C: Naive T cells have a shorter lifespan than memory T cells.
D: Naive T cells can differentiate into memory B cells.
Answer: A: Memory T cells respond more rapidly upon re-exposure to their specific antigen.
41. Long-Term Immunity in Vaccination
What is the primary mechanism by which immunological memory provides long-term protection after vaccination?
A: By constantly producing antibodies in the absence of antigen
B: By preventing the entry of pathogens into the host
C: By maintaining a pool of memory B and T cells that can rapidly respond upon re-exposure to the antigen
D: By inducing inflammation in the absence of infection
Answer: C: By maintaining a pool of memory B and T cells that can rapidly respond upon re-exposure to the antigen
42. Memory B Cells and Their Function
What is the key role of memory B cells in immune responses after vaccination?
A: To secrete cytokines that enhance T cell activity
B: To produce antibodies more rapidly and in larger quantities upon re-exposure to the antigen
C: To act as antigen-presenting cells to naive T cells
D: To promote the destruction of infected cells
Answer: B: To produce antibodies more rapidly and in larger quantities upon re-exposure to the antigen
43. Primary vs. Secondary Immune Response
What is a major difference between the primary immune response and the secondary immune response after vaccination?
A: The secondary immune response is faster and more robust due to the presence of memory cells
B: The primary response involves only T cells, while the secondary response involves both B and T cells
C: The secondary response always leads to the elimination of the pathogen, while the primary response does not
D: The primary response requires booster doses to be effective
Answer: A: The secondary immune response is faster and more robust due to the presence of memory cells
44. Role of Central Memory T Cells
How do central memory T cells differ from effector memory T cells in their role in immune memory?
A: They produce antibodies upon re-exposure to the antigen
B: They remain in peripheral tissues and are ready for immediate action
C: They regulate the immune response by suppressing other immune cells
D: They reside in secondary lymphoid organs and can proliferate upon reactivation
Answer: D: They reside in secondary lymphoid organs and can proliferate upon reactivation
45. Activation of Memory T Cells
What is required for the activation of memory T cells during a secondary immune response?
A: Recognition of the specific antigen they encountered during the initial response
B: Constant exposure to the antigen following vaccination
C: Interaction with plasma cells in lymphoid tissues
D: Activation by regulatory T cells (Tregs)
Answer: A: Recognition of the specific antigen they encountered during the initial response
46. Longevity of Immunological Memory
Which factor primarily determines the longevity of immunological memory after vaccination?
A: The number of initial antigen exposures
B: The strength of the innate immune response
C: The degree of inflammation generated during vaccination
D: The survival of memory B and T cells over time
Answer: D: The survival of memory B and T cells over time
47. Memory T Cells in Mucosal Immunity
Why are memory T cells important for mucosal immunity in the context of vaccination?
A: They produce antibodies that are secreted into mucosal tissues
B: They provide rapid immune responses at mucosal surfaces, preventing pathogen entry
C: They enhance antigen presentation by dendritic cells in mucosal tissues
D: They stimulate long-term inflammation to protect mucosal surfaces
Answer: B: They provide rapid immune responses at mucosal surfaces, preventing pathogen entry
48. Clonal Expansion in Immunological Memory
What happens during the clonal expansion of memory cells following re-exposure to an antigen?
A: Memory cells undergo apoptosis to limit immune activation
B: Memory cells present antigens to other immune cells
C: Memory cells rapidly proliferate, increasing the number of antigen-specific cells to combat the infection
D: Memory cells differentiate into innate immune cells
Answer: C: Memory cells rapidly proliferate, increasing the number of antigen-specific cells to combat the infection
49. Impact of Antigenic Variation on Immunological Memory
How does antigenic variation in pathogens affect the effectiveness of immunological memory from vaccination?
A: It increases the strength of the immune response
B: It reduces the need for booster vaccinations
C: It enhances memory cell production against the variant
D: It may allow the pathogen to evade immune recognition, reducing vaccine effectiveness
Answer: D: It may allow the pathogen to evade immune recognition, reducing vaccine effectiveness
50. Role of Memory Plasma Cells
What is the primary function of memory plasma cells in long-term immunity?
A: To continuously produce antibodies specific to the original antigen
B: To act as antigen-presenting cells
C: To stimulate naive B cells to differentiate
D: To produce cytokines that activate T cells
Answer: A: To continuously produce antibodies specific to the original antigen
51. Class Switching in Immunoglobulins
What is the primary significance of class switching in immunoglobulins?
A: It alters the antigen specificity of the antibody
B: It changes the affinity of the antibody for its antigen
C: It allows the immune response to adapt by producing different isotypes without changing antigen specificity
D: It enhances the neutralizing ability of IgM
Answer: C: It allows the immune response to adapt by producing different isotypes without changing antigen specificity
52. Function of IgE in Allergic Reactions
Which of the following describes the primary role of IgE in allergic reactions?
A: Neutralizing bacterial toxins
B: Binding to mast cells and basophils, triggering histamine release upon antigen exposure
C: Opsonizing pathogens for phagocytosis
D: Activating the complement system directly
Answer: B: Binding to mast cells and basophils, triggering histamine release upon antigen exposure
53. First Antibody Produced in Response to Infection
Which immunoglobulin class is typically the first to be produced during a primary immune response?
A: IgM
B: IgG
C: IgA
D: IgE
Answer: A: IgM
54. Role of the J Chain in Immunoglobulins
What is the primary role of the J chain in immunoglobulins?
A: It enhances antigen binding to IgG molecules
B: It facilitates antigen presentation to T cells
C: It binds IgE to mast cells
D: It links monomers of IgA and IgM to form dimers or pentamers
Answer: D: It links monomers of IgA and IgM to form dimers or pentamers
55. Mucosal Immunity and IgA
What is the primary function of IgA in mucosal immunity?
A: Neutralizing pathogens at mucosal surfaces
B: Triggering histamine release during allergic reactions
C: Activating the classical complement pathway
D: Facilitating phagocytosis by macrophages
Answer: A: Neutralizing pathogens at mucosal surfaces
56. IgG and Placental Transfer
Why is IgG unique among immunoglobulins in its ability to cross the placenta?
A: It binds to a receptor on placental cells that allows it to transfer from maternal to fetal circulation
B: It has a higher affinity for antigens than other immunoglobulins
C: It is the smallest immunoglobulin and can pass through pores in the placenta
D: It interacts with Fc receptors that mediate transport across the placental barrier
Answer: D: It interacts with Fc receptors that mediate transport across the placental barrier
57. Opsonization and Immunoglobulins
Which immunoglobulin class is most effective at opsonization?
A: IgM
B: IgG
C: IgE
D: IgA
Answer: B: IgG
58. Complement Activation by IgM
Why is IgM particularly effective at activating the complement system?
A: It binds to mast cells and releases inflammatory mediators
B: It has a high affinity for antigens and binds them tightly
C: It forms pentamers, allowing for efficient binding to C1q, the first component of the classical complement pathway
D: It neutralizes viruses before they can infect cells
Answer: C: It forms pentamers, allowing for efficient binding to C1q, the first component of the classical complement pathway
59. Function of IgD in the Immune Response
What is the primary function of IgD in the immune system?
A: Neutralizing pathogens in the bloodstream
B: Binding to basophils and initiating allergic responses
C: Cross-linking with antigens to trigger the complement cascade
D: Acting as a receptor on the surface of B cells to initiate activation
Answer: D: Acting as a receptor on the surface of B cells to initiate activation
60. Affinity Maturation in Immunoglobulins
What process allows for increased affinity of antibodies during the immune response?
A: Somatic hypermutation in the variable regions of the antibody genes
B: Class switching to different isotypes
C: Production of additional light chain variants
D: Increased binding of IgE to mast cells
Answer: A: Somatic hypermutation in the variable regions of the antibody genes
61. Classical Pathway Activation
Which of the following primarily activates the classical pathway of the complement system?
A: Direct binding of microbial surfaces to complement proteins
B: Release of cytokines during inflammation
C: Antigen-antibody complexes binding to C1
D: Bacterial endotoxins
Answer: C: Antigen-antibody complexes binding to C1
62. Role of C3 Convertase in the Complement System
What is the main function of C3 convertase in the complement cascade?
A: To bind directly to pathogens for opsonization
B: To cleave C3 into C3a and C3b, amplifying the complement response
C: To recruit macrophages to the site of infection
D: To promote blood clotting during inflammation
Answer: B: To cleave C3 into C3a and C3b, amplifying the complement response
63. Lectin Pathway Activation
How is the lectin pathway of complement activation initiated?
A: By mannose-binding lectin binding to carbohydrates on microbial surfaces
B: By the spontaneous activation of C3 in the blood
C: By the presence of antigen-antibody complexes
D: By direct interaction with natural killer cells
Answer: A: By mannose-binding lectin binding to carbohydrates on microbial surfaces
64. Terminal Complement Complex (MAC) Function
What is the primary role of the membrane attack complex (MAC) in the complement system?
A: To enhance phagocytosis by immune cells
B: To neutralize viruses through binding
C: To initiate an inflammatory response
D: To form pores in the cell membranes of pathogens, leading to lysis
Answer: D: To form pores in the cell membranes of pathogens, leading to lysis
65. Role of C5a in Inflammation
How does the complement protein C5a contribute to the immune response?
A: By acting as a potent chemoattractant for neutrophils
B: By lysing bacterial cell walls
C: By directly opsonizing pathogens
D: By inhibiting T-cell activation
Answer: A: By acting as a potent chemoattractant for neutrophils
66. Regulation of Complement Activity by Factor I
What is the role of complement regulatory protein Factor I?
A: To promote the activation of the alternative pathway
B: To stabilize the C3 convertase on microbial surfaces
C: To recruit T cells to the site of infection
D: To inactivate C3b and C4b, preventing excessive complement activation
Answer: D: To inactivate C3b and C4b, preventing excessive complement activation
67. Alternative Pathway of Complement Activation
What is the unique feature of the alternative pathway of complement activation compared to the classical pathway?
A: It requires antibodies to initiate the response
B: It is activated spontaneously on microbial surfaces without the need for antibodies
C: It activates natural killer cells directly
D: It involves the release of cytokines before complement activation
Answer: B: It is activated spontaneously on microbial surfaces without the need for antibodies
68. Anaphylatoxins and Their Role in Immune Response
Which complement components are classified as anaphylatoxins and what is their function?
A: C1 and C2; they activate T cells
B: C3b and C5b; they promote opsonization
C: C3a, C4a, and C5a; they enhance inflammation by inducing smooth muscle contraction and increasing vascular permeability
D: C6 and C7; they lyse pathogens
Answer: C: C3a, C4a, and C5a; they enhance inflammation by inducing smooth muscle contraction and increasing vascular permeability
69. Deficiency in C1 Inhibitor and Disease
Which condition is associated with a deficiency in C1 inhibitor (C1-INH) in the complement system?
A: Systemic lupus erythematosus
B: Chronic granulomatous disease
C: Rheumatoid arthritis
D: Hereditary angioedema
Answer: D: Hereditary angioedema
70. Opsonization and the Complement System
Which complement component is primarily responsible for opsonization of pathogens, facilitating their clearance by phagocytes?
A: C3b
B: C5a
C: C9
D: C1q
Answer: A: C3b
71. Central Tolerance in the Thymus
How does central tolerance eliminate self-reactive T cells in the thymus?
A: By promoting the differentiation of T cells into regulatory T cells
B: By inducing somatic hypermutation in T cell receptors
C: By inducing apoptosis of T cells that strongly bind self-antigens during negative selection
D: By enhancing the expression of non-self antigens in the thymus
Answer: C: By inducing apoptosis of T cells that strongly bind self-antigens during negative selection
72. Anergy in Peripheral Tolerance
What is the primary outcome when a self-reactive T cell encounters an antigen without costimulation in the periphery?
A: It undergoes clonal expansion and differentiates into an effector T cell
B: It becomes anergic, losing its ability to respond to antigen
C: It migrates to secondary lymphoid tissues and activates B cells
D: It differentiates into a cytotoxic T cell
Answer: B: It becomes anergic, losing its ability to respond to antigen
73. Role of Regulatory T Cells (Tregs)
What is the main function of regulatory T cells (Tregs) in maintaining self-tolerance?
A: To suppress immune responses against self-antigens and prevent autoimmunity
B: To enhance the function of cytotoxic T cells
C: To promote the differentiation of naïve T cells into effector cells
D: To activate B cells to produce autoantibodies
Answer: A: To suppress immune responses against self-antigens and prevent autoimmunity
74. Mechanism of Peripheral Tolerance in B Cells
How is peripheral tolerance achieved in B cells that recognize self-antigens in the absence of T cell help?
A: By promoting somatic hypermutation in the B cell receptor
B: By activating the complement system
C: By enhancing the presentation of antigens to helper T cells
D: By inducing B cell anergy or apoptosis
Answer: D: By inducing B cell anergy or apoptosis
75. Function of Clonal Deletion in Tolerance
What is the purpose of clonal deletion in the development of immune tolerance?
A: To eliminate self-reactive lymphocytes during their development
B: To enhance the proliferation of immune cells
C: To activate memory T cells against self-antigens
D: To inhibit the function of antigen-presenting cells
Answer: A: To eliminate self-reactive lymphocytes during their development
76. Role of AIRE in Central Tolerance
How does the Autoimmune Regulator (AIRE) gene contribute to central tolerance in the thymus?
A: By inhibiting the expression of tissue-specific antigens
B: By enhancing the selection of autoreactive T cells
C: By promoting the migration of T cells to the periphery
D: By promoting the expression of tissue-specific antigens in the thymus for negative selection
Answer: D: By promoting the expression of tissue-specific antigens in the thymus for negative selection
77. Molecular Mimicry and Autoimmunity
How does molecular mimicry contribute to the development of autoimmunity?
A: It allows immune cells to recognize both self and foreign antigens
B: It occurs when foreign antigens resemble self-antigens, leading to an immune response against self
C: It enhances immune tolerance by suppressing T cell activation
D: It involves the suppression of regulatory T cell function
Answer: B: It occurs when foreign antigens resemble self-antigens, leading to an immune response against self
78. Role of Fas-FasL in Immune Homeostasis
What is the role of the Fas-FasL pathway in maintaining immune homeostasis?
A: To promote the activation of T cells in response to self-antigens
B: To induce somatic hypermutation in B cells
C: To trigger apoptosis in activated lymphocytes, preventing autoimmune responses
D: To enhance the production of antibodies by plasma cells
Answer: C: To trigger apoptosis in activated lymphocytes, preventing autoimmune responses
79. Mechanism of Autoimmune Lymphoproliferative Syndrome (ALPS)
What causes Autoimmune Lymphoproliferative Syndrome (ALPS)?
A: Excessive activation of regulatory T cells
B: Enhanced thymic selection of autoreactive T cells
C: Overexpression of tissue-specific antigens in the thymus
D: Defective Fas-mediated apoptosis of self-reactive lymphocytes
Answer: D: Defective Fas-mediated apoptosis of self-reactive lymphocytes
80. Tolerogenic Dendritic Cells in Peripheral Tolerance
How do tolerogenic dendritic cells contribute to peripheral tolerance?
A: By presenting self-antigens to T cells without costimulation, leading to anergy or deletion
B: By promoting the activation of cytotoxic T cells against self-antigens
C: By enhancing the proliferation of autoreactive T cells
D: By stimulating the production of pro-inflammatory cytokines
Answer: A: By presenting self-antigens to T cells without costimulation, leading to anergy or deletion
81. Mechanism of Type I Hypersensitivity
What is the primary mechanism that triggers a Type I hypersensitivity reaction?
A: Activation of cytotoxic T cells
B: Formation of immune complexes between antigen and antibody
C: Cross-linking of IgE antibodies on mast cells and basophils, leading to degranulation
D: Activation of complement proteins
Answer: C: Cross-linking of IgE antibodies on mast cells and basophils, leading to degranulation
82. Type II Hypersensitivity and Tissue Damage
In a Type II hypersensitivity reaction, how is tissue damage primarily mediated?
A: By IgE-mediated histamine release
B: By IgG and IgM antibodies binding to cell surface antigens, leading to complement activation or phagocytosis
C: By immune complexes depositing in tissues
D: By T cell-mediated cytotoxicity
Answer: B: By IgG and IgM antibodies binding to cell surface antigens, leading to complement activation or phagocytosis
83. Type III Hypersensitivity Mechanism
What causes tissue damage in Type III hypersensitivity reactions?
A: Deposition of antigen-antibody complexes in tissues, leading to inflammation
B: Degranulation of mast cells
C: Activation of CD8+ T cells
D: Direct lysis of target cells by antibodies
Answer: A: Deposition of antigen-antibody complexes in tissues, leading to inflammation
84. Type IV Hypersensitivity Timeline
What is characteristic of the delayed onset of a Type IV hypersensitivity reaction?
A: Immediate release of histamine
B: Formation of immune complexes
C: Antibody-mediated cytotoxicity
D: A cell-mediated immune response typically occurring 48-72 hours after antigen exposure
Answer: D: A cell-mediated immune response typically occurring 48-72 hours after antigen exposure
85. Allergic Rhinitis and Hypersensitivity
Allergic rhinitis is primarily associated with which type of hypersensitivity reaction?
A: Type I
B: Type II
C: Type III
D: Type IV
Answer: A: Type I
86. Hemolytic Disease of the Newborn
Hemolytic disease of the newborn (HDN) is an example of which type of hypersensitivity?
A: Type I
B: Type III
C: Type IV
D: Type II
Answer: D: Type II
87. Role of T cells in Type IV Hypersensitivity
In Type IV hypersensitivity reactions, which cell type plays the primary role in mediating the immune response?
A: B cells
B: T cells, particularly CD4+ and CD8+ T cells
C: Mast cells
D: Neutrophils
Answer: B: T cells, particularly CD4+ and CD8+ T cells
88. Serum Sickness and Hypersensitivity
Which hypersensitivity reaction is associated with serum sickness?
A: Type I
B: Type II
C: Type III
D: Type IV
Answer: C: Type III
89. Tuberculin Skin Test and Hypersensitivity
The tuberculin skin test used to diagnose tuberculosis is an example of which type of hypersensitivity reaction?
A: Type I
B: Type II
C: Type III
D: Type IV
Answer: D: Type IV
90. Anaphylaxis and Hypersensitivity
Anaphylaxis is a severe systemic manifestation of which hypersensitivity reaction?
A: Type I
B: Type II
C: Type III
D: Type IV
Answer: A: Type I
91. Cytokine Signaling Pathways
Which of the following is a major signaling pathway activated by cytokine receptors that leads to gene transcription?
A: NF-kB pathway
B: cAMP signaling pathway
C: JAK-STAT pathway
D: MAPK pathway
Answer: C: JAK-STAT pathway
92. Role of IL-2 in Immune Regulation
What is the primary function of interleukin-2 (IL-2) in immune regulation?
A: To suppress immune responses and promote tolerance
B: To stimulate the proliferation of T cells during an immune response
C: To enhance the production of antibodies by B cells
D: To inhibit the activation of macrophages
Answer: B: To stimulate the proliferation of T cells during an immune response
93. Tumor Necrosis Factor-alpha (TNF-α)
How does TNF-α contribute to the immune response during infection?
A: By promoting inflammation and inducing apoptosis of infected cells
B: By increasing the activation of B cells and antibody production
C: By reducing the proliferation of T cells
D: By enhancing the phagocytosis of antigens by neutrophils
Answer: A: By promoting inflammation and inducing apoptosis of infected cells
94. Chemokine Receptor CCR5 and HIV
How does the CCR5 chemokine receptor play a role in HIV infection?
A: It helps the immune system neutralize the virus
B: It induces cytokine production to block viral replication
C: It inhibits HIV from entering host cells
D: It acts as a coreceptor, allowing HIV to enter and infect T cells
Answer: D: It acts as a coreceptor, allowing HIV to enter and infect T cells
95. Interferon-gamma (IFN-γ) Function
What is the primary role of interferon-gamma (IFN-γ) in immune regulation?
A: To activate macrophages and enhance their pathogen-killing abilities
B: To inhibit viral replication in host cells
C: To suppress immune responses during chronic inflammation
D: To increase the activation of B cells and antibody production
Answer: A: To activate macrophages and enhance their pathogen-killing abilities
96. Role of Transforming Growth Factor-beta (TGF-β)
What is the primary immunosuppressive function of TGF-β in the immune system?
A: To activate cytotoxic T lymphocytes (CTLs)
B: To enhance the production of chemokines
C: To promote the production of pro-inflammatory cytokines
D: To inhibit the activation and proliferation of T cells
Answer: D: To inhibit the activation and proliferation of T cells
97. Chemokine CXCL8 (IL-8) in Immune Response
What is the role of CXCL8 (IL-8) in immune responses?
A: To stimulate B cell differentiation
B: To recruit neutrophils to sites of infection or inflammation
C: To inhibit the activity of regulatory T cells
D: To induce apoptosis in virally infected cells
Answer: B: To recruit neutrophils to sites of infection or inflammation
98. IL-10 and Anti-Inflammatory Effects
What is the primary role of interleukin-10 (IL-10) in the immune system?
A: To stimulate the proliferation of T cells and NK cells
B: To promote antibody production by B cells
C: To suppress inflammatory responses and inhibit the activation of macrophages and dendritic cells
D: To enhance cytokine production in pro-inflammatory pathways
Answer: C: To suppress inflammatory responses and inhibit the activation of macrophages and dendritic cells
99. Role of Chemokines in Lymphocyte Trafficking
How do chemokines contribute to lymphocyte trafficking during an immune response?
A: By enhancing cytokine production in target tissues
B: By suppressing T cell activation
C: By reducing the movement of T cells into inflamed tissues
D: By guiding lymphocytes to specific tissues or sites of infection based on chemokine gradients
Answer: D: By guiding lymphocytes to specific tissues or sites of infection based on chemokine gradients
100. IL-1 and Fever Induction
What is the role of IL-1 in the systemic immune response to infection?
A: It induces fever by acting on the hypothalamus
B: It inhibits the release of chemokines from immune cells
C: It suppresses the production of T cells
D: It enhances the activation of natural killer (NK) cells
Answer: A: It induces fever by acting on the hypothalamus
101. Defining Feature of Primary Immunodeficiency
What is the defining characteristic of primary immunodeficiency disorders?
A: They are caused by environmental factors such as infections or chemotherapy
B: They are always associated with autoimmune diseases
C: They are genetically inherited and present early in life
D: They are temporary and resolve without treatment
Answer: C: They are genetically inherited and present early in life
102. Cause of Secondary Immunodeficiencies
Which of the following is a common cause of secondary immunodeficiency disorders?
A: Inherited mutations in immune system genes
B: Acquired factors such as HIV infection or malnutrition
C: Overproduction of immunoglobulins
D: Increased levels of T-cell activation
Answer: B: Acquired factors such as HIV infection or malnutrition
103. Common Presentation of Severe Combined Immunodeficiency (SCID)
How does severe combined immunodeficiency (SCID) typically present in infants?
A: Recurrent, severe infections beginning in early infancy
B: Mild infections that resolve without intervention
C: Overactive immune responses to common antigens
D: Chronic inflammation in the absence of infections
Answer: A: Recurrent, severe infections beginning in early infancy
104. AIDS as a Secondary Immunodeficiency
Why is AIDS considered a secondary immunodeficiency disorder?
A: It is caused by an inherited genetic mutation
B: It primarily affects only B cells
C: It is present at birth and causes severe infections
D: It results from the acquired infection with HIV, which destroys immune cells
Answer: D: It results from the acquired infection with HIV, which destroys immune cells
105. Deficiency of B Cells in Primary Immunodeficiency
In B cell-related primary immunodeficiencies, such as X-linked agammaglobulinemia, what is the primary defect?
A: Failure to produce functional antibodies due to a lack of mature B cells
B: Overproduction of antibodies leading to autoimmunity
C: Excessive proliferation of B cells
D: Impaired T-cell signaling to B cells
Answer: A: Failure to produce functional antibodies due to a lack of mature B cells
106. Treatment for Primary Immunodeficiency
What is the most common treatment approach for patients with primary immunodeficiencies?
A: Broad-spectrum antibiotics
B: Antiviral medications
C: Chemotherapy
D: Immunoglobulin replacement therapy and bone marrow transplantation
Answer: D: Immunoglobulin replacement therapy and bone marrow transplantation
107. Common Secondary Immunodeficiency Causes
Which of the following conditions is a leading cause of secondary immunodeficiency?
A: Genetic mutations in T cell receptors
B: Immunosuppressive treatments, such as chemotherapy or corticosteroids
C: Inherited deficiencies in complement proteins
D: Excessive production of cytokines in the immune system
Answer: B: Immunosuppressive treatments, such as chemotherapy or corticosteroids
108. Diagnosis of Immunodeficiency Disorders
What diagnostic test is typically used to evaluate immunodeficiency disorders?
A: Genetic testing for known mutations
B: Complete blood count (CBC) to measure red blood cells
C: Flow cytometry to assess lymphocyte populations and function
D: Serum protein electrophoresis
Answer: C: Flow cytometry to assess lymphocyte populations and function
109. Opportunistic Infections in Immunodeficiency
Why are individuals with immunodeficiency disorders more susceptible to opportunistic infections?
A: Their immune systems produce too many antibodies
B: Their neutrophils are hyperactive, causing tissue damage
C: Their immune systems are overactive, leading to constant inflammation
D: Their weakened immune systems cannot control normally harmless organisms
Answer: D: Their weakened immune systems cannot control normally harmless organisms
110. Gene Therapy in Immunodeficiency Treatment
What is the role of gene therapy in the treatment of certain primary immunodeficiencies, such as SCID?
A: To correct the genetic defect causing the disorder
B: To stimulate the immune system to overproduce antibodies
C: To suppress the immune response to prevent autoimmunity
D: To prevent infections through vaccination
Answer: A: To correct the genetic defect causing the disorder
111. Mechanism of Subunit Vaccines
How do subunit vaccines provide immunity against specific pathogens?
A: By introducing inactivated whole pathogens to stimulate a full immune response
B: By using live, attenuated forms of the pathogen to induce both humoral and cell-mediated immunity
C: By presenting isolated antigens of the pathogen to stimulate an immune response without causing disease
D: By using viral vectors to deliver the pathogen’s genetic material
Answer: C: By presenting isolated antigens of the pathogen to stimulate an immune response without causing disease
112. Vaccine Adjuvants
What is the main purpose of adding an adjuvant to a vaccine formulation?
A: To inactivate the antigen and make it safer for administration
B: To enhance the immune system's response to the vaccine antigen
C: To decrease the production costs of the vaccine
D: To eliminate the need for booster shots
Answer: B: To enhance the immune system's response to the vaccine antigen
113. Principle of Live Attenuated Vaccines
What is the primary mechanism by which live attenuated vaccines generate immunity?
A: By mimicking a natural infection and inducing both humoral and cellular immunity
B: By inducing the production of memory B cells only
C: By preventing the replication of the pathogen in the host
D: By inhibiting the pathogen’s entry into host cells
Answer: A: By mimicking a natural infection and inducing both humoral and cellular immunity
114. Limitations of Inactivated Vaccines
What is a significant limitation of inactivated vaccines compared to live attenuated vaccines?
A: They can cause disease in immunocompromised individuals
B: They provide lifelong immunity with one dose
C: They typically stimulate stronger cellular immune responses
D: They usually require multiple doses or booster shots to maintain immunity
Answer: D: They usually require multiple doses or booster shots to maintain immunity
115. Mechanism of DNA Vaccines
How do DNA vaccines stimulate the immune system?
A: By delivering genetic material that encodes for pathogen antigens, leading to their expression and subsequent immune response
B: By using inactivated viruses to trigger antibody production
C: By using live, attenuated bacteria to induce an immune response
D: By incorporating recombinant proteins into the immune system
Answer: A: By delivering genetic material that encodes for pathogen antigens, leading to their expression and subsequent immune response
116. Immunological Basis for Conjugate Vaccines
Why are conjugate vaccines particularly effective in infants and young children?
A: They contain live, weakened forms of the pathogen
B: They can elicit a strong immune response without the need for adjuvants
C: They do not require memory cell formation to be effective
D: They link polysaccharides to proteins, enhancing the immune system’s ability to recognize the antigen
Answer: D: They link polysaccharides to proteins, enhancing the immune system’s ability to recognize the antigen
117. Role of B Cells in Vaccine Response
Which process involves B cells in the immune response to vaccination?
A: Direct attack on infected host cells
B: Production of antibodies specific to the vaccine antigen
C: Secretion of cytokines to stimulate other immune cells
D: Activation of the complement system
Answer: B: Production of antibodies specific to the vaccine antigen
118. Immune Memory Induced by Vaccines
What is the primary role of memory cells in vaccine-induced immunity?
A: To generate an immediate immune response upon vaccination
B: To prevent the spread of the pathogen within the host
C: To provide long-lasting immunity by responding quickly upon subsequent exposure to the pathogen
D: To eliminate residual antigens from the vaccination
Answer: C: To provide long-lasting immunity by responding quickly upon subsequent exposure to the pathogen
119. Challenge with Developing Vaccines for RNA Viruses
What is a primary challenge in developing effective vaccines for RNA viruses, such as influenza or HIV?
A: The inability of RNA viruses to replicate in host cells
B: The low mutation rate of RNA viruses
C: The lack of suitable adjuvants for RNA vaccines
D: The high mutation rate of RNA viruses, leading to antigenic variation
Answer: D: The high mutation rate of RNA viruses, leading to antigenic variation
120. Mechanism of Recombinant Vector Vaccines
How do recombinant vector vaccines work to elicit an immune response?
A: By using a harmless virus or bacterium to deliver pathogen antigens to the host’s cells
B: By incorporating whole pathogens into the vaccine to stimulate immunity
C: By providing live attenuated viruses that directly replicate in host cells
D: By stimulating antibody production without introducing the pathogen into the host
Answer: A: By using a harmless virus or bacterium to deliver pathogen antigens to the host’s cells
121. Role of Secretory IgA (sIgA) in Mucosal Immunity
What is the primary function of secretory IgA in the mucosal surfaces, including the oral cavity?
A: To activate complement and induce inflammation
B: To lyse bacterial cells directly
C: To neutralize pathogens and prevent their adherence to epithelial surfaces
D: To enhance the proliferation of immune cells at mucosal surfaces
Answer: C: To neutralize pathogens and prevent their adherence to epithelial surfaces
122. IgA Transport Across Epithelial Cells
How is secretory IgA transported across epithelial cells into the mucosal surface?
A: By passive diffusion through tight junctions
B: Through the polymeric immunoglobulin receptor (pIgR) pathway
C: Via endocytosis and subsequent degradation
D: By active transport using sodium-potassium ATPase
Answer: B: Through the polymeric immunoglobulin receptor (pIgR) pathway
123. Source of Secretory Component in sIgA
What is the origin of the secretory component found in secretory IgA (sIgA)?
A: It is produced by plasma cells in the mucosal tissue
B: It is derived from the epithelial cells as part of the pIgR
C: It is synthesized by macrophages in the mucosal lining
D: It is secreted by dendritic cells during antigen presentation
Answer: A: It is produced by plasma cells in the mucosal tissue
124. Defensive Role of Saliva in the Oral Cavity
Apart from sIgA, how does saliva contribute to mucosal immunity in the oral cavity?
A: By promoting bacterial growth to maintain normal flora
B: By acting as a physical barrier against pathogens
C: By neutralizing toxins produced by pathogenic bacteria
D: By containing antimicrobial proteins like lysozyme and lactoferrin
Answer: D: By containing antimicrobial proteins like lysozyme and lactoferrin
125. IgA Deficiency and Oral Health
What is a common consequence of selective IgA deficiency in the oral cavity?
A: Increased susceptibility to mucosal infections
B: Enhanced secretion of other immunoglobulins
C: Lower levels of microbial colonization
D: Higher concentration of pro-inflammatory cytokines
Answer: A: Increased susceptibility to mucosal infections
126. Polymeric Nature of Secretory IgA
Why is secretory IgA typically found as a dimer at mucosal surfaces?
A: Because dimers have higher affinity for antigen than monomers
B: To allow for rapid activation of the complement system
C: To enhance the inflammatory response at mucosal surfaces
D: Because dimeric sIgA is more resistant to enzymatic degradation
Answer: D: Because dimeric sIgA is more resistant to enzymatic degradation
127. sIgA and Pathogen Neutralization
How does secretory IgA neutralize pathogens in the oral cavity without causing inflammation?
A: By activating complement and recruiting neutrophils
B: By trapping pathogens in mucus and preventing their adherence to epithelial cells
C: By inducing apoptosis in infected epithelial cells
D: By producing pro-inflammatory cytokines
Answer: B: By trapping pathogens in mucus and preventing their adherence to epithelial cells
128. Role of Gut-Associated Lymphoid Tissue (GALT) in IgA Production
How does the gut-associated lymphoid tissue (GALT) contribute to IgA production at mucosal surfaces, including the oral cavity?
A: By secreting IgG antibodies in response to infection
B: By inducing systemic immune responses
C: By priming B cells to secrete IgA, which is then transported to mucosal surfaces
D: By promoting local inflammation and tissue damage
Answer: C: By priming B cells to secrete IgA, which is then transported to mucosal surfaces
129. IgA and Commensal Bacteria in the Oral Cavity
What role does secretory IgA play in maintaining a balanced microbiome in the oral cavity?
A: It selectively destroys pathogenic bacteria
B: It increases the production of antimicrobial peptides
C: It promotes inflammation to reduce microbial colonization
D: It binds to commensal bacteria to limit their overgrowth without inducing an inflammatory response
Answer: D: It binds to commensal bacteria to limit their overgrowth without inducing an inflammatory response
130. Oral Vaccines and IgA Production
How do oral vaccines stimulate the production of IgA in the mucosal immune system?
A: By inducing antigen presentation in the mucosa, leading to the activation of IgA-producing B cells
B: By directly increasing the number of dendritic cells at mucosal surfaces
C: By stimulating systemic IgM production, which triggers IgA release
D: By bypassing the immune system and promoting passive immunity
Answer: A: By inducing antigen presentation in the mucosa, leading to the activation of IgA-producing B cells
131. Antigen-Antibody Complex Formation
What is the primary force that stabilizes antigen-antibody interactions?
A: Covalent bonding between antigen and antibody
B: Hydrogen bonding between antibody heavy and light chains
C: Non-covalent interactions such as hydrogen bonds, electrostatic forces, and van der Waals forces
D: The enzymatic activity of antibodies on antigens
Answer: C: Non-covalent interactions such as hydrogen bonds, electrostatic forces, and van der Waals forces
132. Affinity and Avidity in Antigen-Antibody Binding
What is the main difference between affinity and avidity in antigen-antibody interactions?
A: Affinity refers to the overall strength of binding of multiple antigen-antibody sites
B: Affinity refers to the strength of binding between a single antigen and antibody binding site, while avidity refers to the overall binding strength of an antibody with multiple antigen sites
C: Avidity refers to the ability of antibodies to undergo clonal expansion in response to antigen
D: Affinity is dependent on the number of epitopes, while avidity is not
Answer: B: Affinity refers to the strength of binding between a single antigen and antibody binding site, while avidity refers to the overall binding strength of an antibody with multiple antigen sites
133. Role of the Fab Region in Antigen Recognition
What role does the Fab region of an antibody play in antigen recognition?
A: It binds specifically to the antigen’s epitope, determining the specificity of the immune response
B: It induces a conformational change in the antigen upon binding
C: It mediates effector functions such as complement activation
D: It determines the class of the antibody (e.g., IgG, IgM)
Answer: A: It binds specifically to the antigen’s epitope, determining the specificity of the immune response
134. Agglutination in Diagnostic Tests
What is the primary use of agglutination reactions in diagnostic tests?
A: To identify antigen-antibody complexes under fluorescent light
B: To quantify the concentration of free antibodies in serum
C: To determine the tertiary structure of antibodies
D: To detect the presence of particulate antigens or antibodies by visible clumping
Answer: D: To detect the presence of particulate antigens or antibodies by visible clumping
135. Antigenic Determinants and Antibody Binding
Which component of an antigen is specifically recognized by an antibody?
A: Epitope
B: Paratope
C: Fc region
D: Light chain
Answer: A: Epitope
136. Precipitation Reactions in Immunodiagnostics
In immunoprecipitation assays, what happens when the concentration of antigen and antibody are equivalent?
A: No immune complexes form
B: Only small immune complexes form
C: Antigen is degraded
D: Large, insoluble antigen-antibody complexes form, leading to visible precipitation
Answer: D: Large, insoluble antigen-antibody complexes form, leading to visible precipitation
137. Western Blotting and Antibody Detection
What is the primary purpose of using antibodies in Western blotting?
A: To separate proteins based on size
B: To specifically detect and bind to target proteins that have been separated by electrophoresis
C: To induce protein folding after denaturation
D: To determine the structure of DNA
Answer: B: To specifically detect and bind to target proteins that have been separated by electrophoresis
138. ELISA in Quantifying Antigen-Antibody Reactions
How does an enzyme-linked immunosorbent assay (ELISA) quantify antigen-antibody interactions?
A: By measuring the rate of antigen binding
B: By detecting the release of immune complexes in serum
C: By using an enzyme-linked antibody that produces a color change upon substrate conversion, indicating the presence of antigen or antibody
D: By inducing the release of cytokines
Answer: C: By using an enzyme-linked antibody that produces a color change upon substrate conversion, indicating the presence of antigen or antibody
139. Cross-Reactivity in Antigen-Antibody Interactions
What is cross-reactivity in the context of antigen-antibody interactions?
A: When an antibody binds exclusively to a single antigen
B: When an antigen is degraded before antibody binding
C: When an antibody binds to both antigen and complement proteins
D: When an antibody reacts with multiple antigens due to shared or similar epitopes
Answer: D: When an antibody reacts with multiple antigens due to shared or similar epitopes
140. Monoclonal Antibodies in Diagnostic Testing
Why are monoclonal antibodies particularly useful in diagnostic testing?
A: Because they bind to a single, specific epitope with high specificity
B: Because they trigger stronger immune responses
C: Because they bind to multiple epitopes on different antigens
D: Because they can alter the genetic material of the antigen
Answer: A: Because they bind to a single, specific epitope with high specificity
141. Antigenic Variation in Pathogen Immune Evasion
How does antigenic variation assist pathogens in evading the host immune system?
A: By increasing pathogen replication within host cells
B: By forming biofilms that shield the pathogen from immune detection
C: By altering surface proteins to avoid recognition by antibodies and immune cells
D: By producing enzymes that degrade immune cells
Answer: C: By altering surface proteins to avoid recognition by antibodies and immune cells
142. Role of Latency in Viral Immune Evasion
How does viral latency enable viruses like Herpes simplex to evade the host immune system?
A: By continuously replicating at low levels to avoid detection
B: By remaining dormant in host cells, avoiding immune recognition
C: By suppressing host immune responses through cytokine release
D: By producing proteins that inhibit antigen presentation
Answer: B: By remaining dormant in host cells, avoiding immune recognition
143. Inhibition of Phagocytosis by Bacterial Capsules
How do bacterial capsules help pathogens evade the immune system?
A: By preventing phagocytosis by immune cells
B: By increasing the production of bacterial toxins
C: By enhancing bacterial motility within the host
D: By forming resistant spores
Answer: A: By preventing phagocytosis by immune cells
144. Superantigen Production and Immune Evasion
How do bacterial superantigens contribute to immune evasion?
A: By blocking antibody binding to bacterial surfaces
B: By suppressing immune cell recruitment to the site of infection
C: By inducing rapid bacterial replication in host tissues
D: By causing nonspecific T-cell activation, leading to immune system overload
Answer: D: By causing nonspecific T-cell activation, leading to immune system overload
145. Intracellular Survival of Mycobacterium tuberculosis
How does Mycobacterium tuberculosis evade the immune response after being phagocytosed by macrophages?
A: By inhibiting the fusion of the phagosome with the lysosome
B: By escaping from the phagosome into the cytosol
C: By secreting enzymes that degrade the phagosome membrane
D: By altering its surface proteins to evade immune detection
Answer: A: By inhibiting the fusion of the phagosome with the lysosome
146. Downregulation of MHC Class I by Viruses
How do certain viruses, such as cytomegalovirus, evade cytotoxic T lymphocytes?
A: By mutating rapidly to avoid immune recognition
B: By infecting cells that lack MHC molecules
C: By replicating exclusively in immune-privileged sites
D: By downregulating MHC class I molecules, preventing antigen presentation
Answer: D: By downregulating MHC class I molecules, preventing antigen presentation
147. Biofilm Formation in Bacterial Immune Evasion
What advantage does biofilm formation provide bacteria in terms of immune evasion?
A: It enhances bacterial motility and dissemination
B: It shields bacteria from phagocytosis and antimicrobial agents
C: It increases the speed of bacterial replication
D: It decreases the expression of virulence factors
Answer: B: It shields bacteria from phagocytosis and antimicrobial agents
148. Decoy Receptors in Viral Immune Evasion
How do some viruses use decoy receptors to evade the host immune response?
A: By binding to host immune cells and triggering apoptosis
B: By mimicking host cell receptors and redirecting the immune response
C: By binding to host immune molecules, preventing them from recognizing the actual pathogen
D: By blocking cytokine signaling pathways
Answer: C: By binding to host immune molecules, preventing them from recognizing the actual pathogen
149. Inhibition of Complement Activation by Pathogens
How do certain pathogens inhibit the activation of the complement system?
A: By producing proteins that degrade complement components
B: By inducing mutations in host complement proteins
C: By reducing the expression of complement receptors on immune cells
D: By binding complement regulatory proteins to their surface, preventing complement activation
Answer: D: By binding complement regulatory proteins to their surface, preventing complement activation
150. Molecular Mimicry in Immune Evasion
What is the role of molecular mimicry in pathogen immune evasion?
A: Pathogens produce antigens similar to host molecules, reducing immune recognition
B: Pathogens increase the rate of mutation to escape immune detection
C: Pathogens degrade host antibodies to evade the immune response
D: Pathogens replicate within immune cells to avoid detection
Answer: A: Pathogens produce antigens similar to host molecules, reducing immune recognition
151. Checkpoint Inhibitors in Cancer Immunotherapy
How do checkpoint inhibitors enhance the immune response against cancer cells?
A: By directly killing cancer cells
B: By activating cancer-specific B cells
C: By blocking inhibitory signals that prevent T-cells from attacking cancer cells
D: By increasing the production of cytokines by macrophages
Answer: C: By blocking inhibitory signals that prevent T-cells from attacking cancer cells
152. Monoclonal Antibodies in Cancer Treatment
What is the primary role of monoclonal antibodies in cancer immunotherapy?
A: They enhance antigen presentation by dendritic cells
B: They target specific antigens on cancer cells, leading to immune-mediated destruction
C: They boost the production of immune cells in the bone marrow
D: They reduce tumor growth by inhibiting angiogenesis
Answer: B: They target specific antigens on cancer cells, leading to immune-mediated destruction
153. Mechanism of CAR T-Cell Therapy
How does CAR T-cell therapy work in treating cancer?
A: By modifying a patient's T-cells to express a chimeric antigen receptor that recognizes tumor-specific antigens
B: By introducing cancer-specific antibodies into the bloodstream
C: By enhancing the production of natural killer cells
D: By using viral vectors to deliver therapeutic genes to cancer cells
Answer: A: By modifying a patient's T-cells to express a chimeric antigen receptor that recognizes tumor-specific antigens
154. Cytokine Release Syndrome (CRS) in Immunotherapy
What causes cytokine release syndrome (CRS) in patients undergoing immunotherapy, such as CAR T-cell therapy?
A: Overproduction of immunosuppressive T regulatory cells
B: Decreased activation of macrophages
C: Inhibition of checkpoint proteins
D: Rapid activation and proliferation of immune cells, leading to excessive cytokine production
Answer: D: Rapid activation and proliferation of immune cells, leading to excessive cytokine production
155. Role of PD-1/PD-L1 in Tumor Immune Evasion
How does the interaction between PD-1 on T-cells and PD-L1 on tumor cells contribute to immune evasion by tumors?
A: It inhibits T-cell activity, allowing tumor cells to avoid immune destruction
B: It enhances the proliferation of cancer cells by providing growth signals
C: It promotes T-cell activation, resulting in tumor cell destruction
D: It decreases the ability of macrophages to phagocytose tumor cells
Answer: A: It inhibits T-cell activity, allowing tumor cells to avoid immune destruction
156. Adoptive Cell Transfer in Immunotherapy
What is adoptive cell transfer (ACT) in the context of cancer immunotherapy?
A: The infusion of engineered T-cells to target tumor antigens
B: The administration of checkpoint inhibitors to enhance immune response
C: The use of monoclonal antibodies to destroy cancer cells
D: The collection and expansion of a patient’s own T-cells, which are then reinfused to attack tumors
Answer: D: The collection and expansion of a patient’s own T-cells, which are then reinfused to attack tumors
157. Allergen-Specific Immunotherapy
What is the goal of allergen-specific immunotherapy in treating allergic diseases?
A: To increase IgE production in response to the allergen
B: To reduce immune sensitivity to specific allergens by gradually exposing the patient to increasing doses of the allergen
C: To block histamine release from mast cells
D: To inhibit T-cell activity in response to allergens
Answer: B: To reduce immune sensitivity to specific allergens by gradually exposing the patient to increasing doses of the allergen
158. Role of Regulatory T-Cells in Immunotherapy
How do regulatory T-cells (Tregs) influence the effectiveness of cancer immunotherapy?
A: By directly killing tumor cells
B: By promoting immune activation and inflammation
C: By suppressing the immune response and limiting the effectiveness of the therapy
D: By enhancing antibody production against tumor antigens
Answer: C: By suppressing the immune response and limiting the effectiveness of the therapy
159. Immune Checkpoint Blockade Resistance
What is a common mechanism by which tumors develop resistance to immune checkpoint blockade therapies?
A: Mutations in T-cell receptors
B: Increased expression of tumor-specific antigens
C: Enhanced production of chemokines
D: Upregulation of alternative immune checkpoints
Answer: D: Upregulation of alternative immune checkpoints
160. Desensitization Therapy for Allergies
What is the primary mechanism of desensitization therapy in the treatment of allergies?
A: By inducing tolerance through repeated exposure to small amounts of the allergen
B: By increasing the production of IgE antibodies
C: By promoting histamine release in response to allergens
D: By inhibiting the production of cytokines
Answer: A: By inducing tolerance through repeated exposure to small amounts of the allergen
161. Role of Molecular Mimicry in Autoimmune Disease
How does molecular mimicry contribute to the development of autoimmune diseases?
A: By preventing the immune system from recognizing self-antigens
B: By increasing the production of T regulatory cells
C: By causing cross-reactivity between pathogen antigens and host tissues, leading to autoimmunity
D: By directly attacking immune cells
Answer: C: By causing cross-reactivity between pathogen antigens and host tissues, leading to autoimmunity
162. Pathogenesis of Rheumatoid Arthritis (RA)
What is a key feature of the pathogenesis of rheumatoid arthritis?
A: The activation of cytotoxic T-cells targeting myelin sheaths
B: The formation of immune complexes and synovial inflammation
C: The destruction of pancreatic beta cells by autoreactive T-cells
D: The overproduction of immunoglobulin G (IgG) leading to tissue damage
Answer: B: The formation of immune complexes and synovial inflammation
163. Autoantibody Production in Systemic Lupus Erythematosus (SLE)
What is the significance of autoantibody production in systemic lupus erythematosus (SLE)?
A: Autoantibodies, such as anti-dsDNA, target nuclear components, leading to widespread tissue damage
B: Autoantibodies neutralize cytokines, causing immunosuppression
C: Autoantibodies increase the clearance of immune complexes from the bloodstream
D: Autoantibodies stimulate the production of regulatory T cells
Answer: A: Autoantibodies, such as anti-dsDNA, target nuclear components, leading to widespread tissue damage
164. Role of Environmental Factors in Autoimmune Disease
Which environmental factor has been implicated in triggering autoimmune diseases in genetically predisposed individuals?
A: Excessive physical exercise
B: High protein diets
C: High altitude exposure
D: Viral infections, such as Epstein-Barr virus (EBV)
Answer: D: Viral infections, such as Epstein-Barr virus (EBV)
165. Function of Regulatory T Cells in Autoimmunity
How do regulatory T cells (Tregs) prevent the development of autoimmune diseases?
A: By suppressing autoreactive T-cells and maintaining immune tolerance
B: By enhancing the activation of cytotoxic T-cells
C: By producing large amounts of antibodies
D: By promoting the proliferation of B cells
Answer: A: By suppressing autoreactive T-cells and maintaining immune tolerance
166. Genetic Susceptibility in Autoimmune Disease
How does the presence of certain HLA alleles influence the risk of developing autoimmune diseases?
A: By preventing the immune system from recognizing pathogens
B: By decreasing the expression of MHC class I molecules
C: By altering the structure of B cell receptors
D: By presenting self-antigens to T cells, leading to autoimmunity
Answer: D: By presenting self-antigens to T cells, leading to autoimmunity
167. Cytokines and Inflammation in Autoimmune Disease
Which cytokine is commonly elevated in autoimmune diseases such as rheumatoid arthritis, contributing to inflammation and joint destruction?
A: IL-4
B: Tumor necrosis factor-alpha (TNF-α)
C: Interferon-gamma (IFN-γ)
D: IL-10
Answer: B: Tumor necrosis factor-alpha (TNF-α)
168. Autoimmune Hemolytic Anemia Pathogenesis
What is the primary mechanism underlying autoimmune hemolytic anemia?
A: The destruction of pancreatic beta cells by autoreactive T cells
B: The production of antibodies that inhibit erythropoiesis
C: The production of autoantibodies that target red blood cells, leading to their destruction
D: The inhibition of platelet production in the bone marrow
Answer: C: The production of autoantibodies that target red blood cells, leading to their destruction
169. Complement Activation in Systemic Lupus Erythematosus (SLE)
How does complement activation contribute to the pathogenesis of systemic lupus erythematosus (SLE)?
A: By preventing immune complex formation
B: By enhancing the clearance of apoptotic cells
C: By blocking B-cell maturation
D: By amplifying inflammation and tissue damage through the formation of membrane attack complexes (MACs)
Answer: D: By amplifying inflammation and tissue damage through the formation of membrane attack complexes (MACs)
170. Antigenic Targets in Multiple Sclerosis (MS)
What is the primary target of the immune response in multiple sclerosis (MS)?
A: The myelin sheath surrounding central nervous system neurons
B: The insulin-producing beta cells of the pancreas
C: The epithelial cells lining the respiratory tract
D: The endothelial cells of blood vessels
Answer: A: The myelin sheath surrounding central nervous system neurons
171. Type I Hypersensitivity Reaction
What immune component is primarily involved in mediating a Type I hypersensitivity reaction, such as anaphylaxis?
A: Cytotoxic T cells
B: IgG antibodies
C: IgE antibodies binding to mast cells and basophils
D: Immune complexes
Answer: C: IgE antibodies binding to mast cells and basophils
172. Role of Histamine in Allergic Reactions
What is the primary effect of histamine release during an allergic reaction?
A: Inducing T-cell proliferation
B: Increasing vascular permeability and causing vasodilation
C: Enhancing the destruction of pathogens by macrophages
D: Blocking the release of cytokines from immune cells
Answer: B: Increasing vascular permeability and causing vasodilation
173. Antigen in Allergic Reactions
What role does the antigen play in the initiation of an allergic reaction?
A: It triggers the initial sensitization by binding to IgE on mast cells
B: It stimulates the production of cytotoxic T cells
C: It binds directly to histamine receptors on immune cells
D: It blocks immune responses to pathogens
Answer: A: It triggers the initial sensitization by binding to IgE on mast cells
174. Late-Phase Allergic Reaction
What causes the late-phase response in allergic reactions?
A: Immediate release of histamine from mast cells
B: IgE antibodies neutralizing the allergen
C: Degranulation of basophils releasing proteolytic enzymes
D: Recruitment of eosinophils and other inflammatory cells to the site of allergen exposure
Answer: D: Recruitment of eosinophils and other inflammatory cells to the site of allergen exposure
175. Anaphylaxis Management
What is the first-line treatment for anaphylaxis?
A: Intramuscular injection of epinephrine
B: Oral antihistamines
C: Intravenous corticosteroids
D: Oxygen therapy
Answer: A: Intramuscular injection of epinephrine
176. Type IV Hypersensitivity Reaction
What differentiates a Type IV hypersensitivity reaction, such as contact dermatitis, from other allergic reactions?
A: It is mediated by IgE antibodies
B: It involves immune complexes
C: It occurs immediately upon exposure to the allergen
D: It is delayed and primarily mediated by T cells
Answer: D: It is delayed and primarily mediated by T cells
177. Use of Corticosteroids in Allergic Reactions
How do corticosteroids manage allergic reactions?
A: By directly neutralizing the allergen
B: By reducing inflammation through inhibition of cytokine production
C: By blocking histamine receptors on immune cells
D: By preventing the binding of IgE to mast cells
Answer: B: By reducing inflammation through inhibition of cytokine production
178. Allergen-Specific Immunotherapy (Desensitization)
What is the primary goal of allergen-specific immunotherapy?
A: To block the release of histamine from mast cells
B: To prevent the production of IgE antibodies
C: To induce immune tolerance by gradually exposing the patient to increasing amounts of the allergen
D: To prevent the activation of complement proteins
Answer: C: To induce immune tolerance by gradually exposing the patient to increasing amounts of the allergen
179. Role of Leukotrienes in Allergic Reactions
How do leukotrienes contribute to the pathophysiology of allergic reactions?
A: By directly deactivating mast cells
B: By blocking histamine release from basophils
C: By neutralizing the allergen in the bloodstream
D: By increasing bronchoconstriction, vascular permeability, and mucus production
Answer: D: By increasing bronchoconstriction, vascular permeability, and mucus production
180. Antihistamines in Allergy Management
How do antihistamines alleviate symptoms of allergic reactions?
A: By blocking histamine receptors, preventing histamine from binding to its target
B: By suppressing IgE production in B cells
C: By inhibiting the recruitment of T cells to the site of allergen exposure
D: By increasing the metabolism of histamine in the liver
Answer: A: By blocking histamine receptors, preventing histamine from binding to its target
181. Regulatory T Cells (Tregs) in Immune Homeostasis
How do regulatory T cells (Tregs) contribute to immune homeostasis?
A: By directly killing pathogens in the bloodstream
B: By enhancing the activation of effector T cells
C: By suppressing the activation and proliferation of autoreactive T cells
D: By promoting the release of pro-inflammatory cytokines
Answer: C: By suppressing the activation and proliferation of autoreactive T cells
182. FoxP3 and Treg Function
What is the role of the transcription factor FoxP3 in regulatory T cells?
A: It promotes the differentiation of effector T cells
B: It is essential for the development and function of Tregs
C: It suppresses the expression of surface markers on Tregs
D: It enhances cytokine production in effector T cells
Answer: B: It is essential for the development and function of Tregs
183. Mechanism of Treg-Mediated Suppression
Which of the following is a key mechanism by which Tregs suppress immune responses?
A: By secreting anti-inflammatory cytokines such as IL-10 and TGF-β
B: By promoting the activation of natural killer (NK) cells
C: By inhibiting the expression of FoxP3 in effector T cells
D: By increasing the production of pro-inflammatory cytokines
Answer: A: By secreting anti-inflammatory cytokines such as IL-10 and TGF-β
184. Role of Tregs in Autoimmune Diseases
How does a deficiency in Tregs contribute to the development of autoimmune diseases?
A: By reducing the proliferation of autoreactive B cells
B: By promoting tolerance to self-antigens
C: By increasing the production of antibodies against pathogens
D: By failing to suppress autoreactive immune cells, leading to tissue damage
Answer: D: By failing to suppress autoreactive immune cells, leading to tissue damage
185. Treg Development in the Thymus
What is the role of the thymus in Treg development?
A: It is where thymic Tregs are selected based on their ability to recognize self-antigens
B: It produces pro-inflammatory cytokines that enhance Treg function
C: It allows for the differentiation of Tregs into effector T cells
D: It prevents the migration of Tregs to peripheral tissues
Answer: A: It is where thymic Tregs are selected based on their ability to recognize self-antigens
186. CTLA-4 and Treg Function
How does CTLA-4 contribute to the immunosuppressive function of Tregs?
A: By enhancing the secretion of IL-2
B: By inhibiting the differentiation of Tregs
C: By increasing Treg proliferation
D: By inhibiting costimulatory signals required for effector T cell activation
Answer: D: By inhibiting costimulatory signals required for effector T cell activation
187. Tregs in Tumor Immunology
What role do Tregs play in the tumor microenvironment?
A: They enhance the activity of cytotoxic T cells
B: They suppress the immune response against tumor cells, promoting tumor growth
C: They promote the migration of immune cells to the tumor site
D: They increase the expression of tumor-specific antigens
Answer: B: They suppress the immune response against tumor cells, promoting tumor growth
188. Peripheral Tolerance and Tregs
How do Tregs maintain peripheral tolerance to self-antigens?
A: By inducing apoptosis in effector T cells
B: By enhancing the differentiation of effector T cells
C: By suppressing autoreactive T cells in peripheral tissues
D: By increasing the activation of dendritic cells
Answer: C: By suppressing autoreactive T cells in peripheral tissues
189. Treg Dysregulation and Inflammatory Diseases
How does dysregulation of Treg function contribute to chronic inflammatory diseases?
A: By increasing the production of IL-10
B: By promoting the clearance of infections
C: By enhancing the differentiation of Tregs into effector T cells
D: By failing to suppress pro-inflammatory responses, leading to tissue damage
Answer: D: By failing to suppress pro-inflammatory responses, leading to tissue damage
190. Therapeutic Targeting of Tregs in Autoimmune Diseases
How can enhancing Treg function be a potential therapeutic strategy for autoimmune diseases?
A: By promoting immune tolerance and reducing inflammation
B: By increasing the activity of effector T cells against self-antigens
C: By inhibiting Treg migration to affected tissues
D: By decreasing the production of anti-inflammatory cytokines
Answer: A: By promoting immune tolerance and reducing inflammation
191. Role of T Cells in Periodontitis
How do T cells contribute to the pathogenesis of periodontitis?
A: By producing cytokines that promote tissue regeneration
B: By preventing the activation of B cells and antibody production
C: By releasing pro-inflammatory cytokines that drive tissue destruction
D: By inhibiting neutrophil migration to the site of infection
Answer: C: By releasing pro-inflammatory cytokines that drive tissue destruction
192. Neutrophil Function in Gingivitis
What is the primary role of neutrophils in gingivitis?
A: To promote tissue repair by releasing growth factors
B: To act as the first line of defense by phagocytosing bacteria in the gingival crevice
C: To secrete antibodies that neutralize bacterial toxins
D: To prevent the migration of lymphocytes to the inflamed site
Answer: B: To act as the first line of defense by phagocytosing bacteria in the gingival crevice
193. Cytokine Release in Gingival Inflammation
Which cytokine is most commonly associated with promoting inflammation in gingivitis?
A: Interleukin-1 (IL-1)
B: Tumor necrosis factor-alpha (TNF-α)
C: Interleukin-10 (IL-10)
D: Transforming growth factor-beta (TGF-β)
Answer: A: Interleukin-1 (IL-1)
194. Antibody Response in Chronic Periodontitis
What role do antibodies play in chronic periodontitis?
A: They neutralize bacterial toxins and prevent further infection
B: They promote phagocytosis by binding to bacterial surface antigens
C: They block inflammatory signaling pathways
D: They are ineffective at halting tissue destruction and may contribute to disease progression
Answer: D: They are ineffective at halting tissue destruction and may contribute to disease progression
195. Role of Matrix Metalloproteinases (MMPs) in Periodontitis
How do matrix metalloproteinases (MMPs) contribute to tissue destruction in periodontitis?
A: By degrading the extracellular matrix components such as collagen
B: By stimulating the proliferation of fibroblasts
C: By preventing the migration of immune cells to the site of infection
D: By enhancing the production of anti-inflammatory cytokines
Answer: A: By degrading the extracellular matrix components such as collagen
196. Th17 Cells in Periodontal Disease
What is the role of Th17 cells in the immune response during periodontal disease?
A: They prevent bacterial adhesion to gingival tissues
B: They suppress immune responses to maintain homeostasis
C: They promote tissue regeneration through growth factor release
D: They contribute to inflammation by secreting IL-17, which recruits neutrophils and enhances tissue destruction
Answer: D: They contribute to inflammation by secreting IL-17, which recruits neutrophils and enhances tissue destruction
197. Bacterial Biofilm and Host Immune Response
How does the presence of bacterial biofilms in the gingival sulcus affect the host immune response in periodontitis?
A: It reduces the immune response by preventing immune cell migration
B: It enhances the chronic inflammatory response by continuously activating immune cells
C: It neutralizes the activity of neutrophils and macrophages
D: It prevents the activation of T cells in the periodontal pocket
Answer: B: It enhances the chronic inflammatory response by continuously activating immune cells
198. Role of Regulatory T Cells (Tregs) in Periodontal Health
How do regulatory T cells (Tregs) contribute to periodontal health?
A: By stimulating neutrophil activity
B: By promoting bone resorption through cytokine production
C: By suppressing excessive immune responses and preventing tissue damage
D: By enhancing antibody production against periodontal pathogens
Answer: C: By suppressing excessive immune responses and preventing tissue damage
199. Osteoclast Activity in Periodontitis
What is the primary mechanism through which osteoclasts contribute to bone loss in periodontitis?
A: By degrading the surrounding soft tissue
B: By enhancing the proliferation of fibroblasts
C: By stimulating the production of anti-inflammatory cytokines
D: By resorbing alveolar bone in response to inflammatory cytokines like RANKL
Answer: D: By resorbing alveolar bone in response to inflammatory cytokines like RANKL
200. Role of IL-10 in Periodontal Inflammation
How does the anti-inflammatory cytokine IL-10 affect periodontal disease progression?
A: By downregulating pro-inflammatory cytokine production and limiting tissue destruction
B: By enhancing the recruitment of neutrophils to the site of infection
C: By promoting bacterial adhesion to gingival tissues
D: By increasing collagen degradation in the periodontal ligament
Answer: A: By downregulating pro-inflammatory cytokine production and limiting tissue destruction
201. Mechanism of Action of Monoclonal Antibodies
How do monoclonal antibodies primarily exert their therapeutic effects?
A: By directly killing cancer cells
B: By neutralizing toxins produced by pathogens
C: By specifically binding to antigens on target cells, marking them for destruction by the immune system
D: By blocking all protein synthesis in the target cell
Answer: C: By specifically binding to antigens on target cells, marking them for destruction by the immune system
202. Humanization of Monoclonal Antibodies
Why are many monoclonal antibodies "humanized" before therapeutic use in humans?
A: To increase their ability to bind to human antigens
B: To reduce the immune response against the antibody itself
C: To increase their half-life in the bloodstream
D: To enhance their ability to cross the blood-brain barrier
Answer: B: To reduce the immune response against the antibody itself
203. Targeted Therapy in Cancer
How do monoclonal antibodies function as targeted therapies in cancer treatment?
A: By specifically binding to cancer cell antigens and blocking cell growth or inducing apoptosis
B: By increasing the sensitivity of cancer cells to chemotherapy
C: By activating T cells to attack healthy cells
D: By directly enhancing the proliferation of normal cells
Answer: A: By specifically binding to cancer cell antigens and blocking cell growth or inducing apoptosis
204. Mechanism of Immune Checkpoint Inhibitors
What is the mechanism by which monoclonal antibodies targeting immune checkpoints, such as PD-1 or CTLA-4, enhance anti-tumor immunity?
A: By preventing tumor cells from producing toxins
B: By increasing the number of regulatory T cells
C: By increasing the production of antibodies against tumor cells
D: By blocking inhibitory signals that prevent T cells from attacking tumor cells
Answer: D: By blocking inhibitory signals that prevent T cells from attacking tumor cells
205. Antibody-Drug Conjugates (ADCs)
What is the therapeutic advantage of antibody-drug conjugates (ADCs)?
A: They deliver cytotoxic drugs directly to cancer cells via antibody targeting, minimizing damage to normal cells
B: They enhance the immune system’s ability to detect cancer cells
C: They prevent angiogenesis in tumor environments
D: They increase the half-life of chemotherapeutic agents
Answer: A: They deliver cytotoxic drugs directly to cancer cells via antibody targeting, minimizing damage to normal cells
206. Monoclonal Antibodies in Autoimmune Diseases
How do monoclonal antibodies used to treat autoimmune diseases, such as rheumatoid arthritis, function?
A: By enhancing immune cell activity against autoantigens
B: By increasing the production of inflammatory cytokines
C: By promoting the proliferation of T cells
D: By blocking specific immune system molecules involved in the inflammatory response, such as TNF-α
Answer: D: By blocking specific immune system molecules involved in the inflammatory response, such as TNF-α
207. Antibody-Dependent Cellular Cytotoxicity (ADCC)
What is the role of antibody-dependent cellular cytotoxicity (ADCC) in the action of therapeutic monoclonal antibodies?
A: It directly induces apoptosis in tumor cells
B: It involves the recruitment of immune cells like natural killer cells to destroy antibody-coated target cells
C: It prevents the spread of cancer to other tissues
D: It increases the production of cytokines in the target cell
Answer: B: It involves the recruitment of immune cells like natural killer cells to destroy antibody-coated target cells
208. Chimeric Antigen Receptor (CAR) T-Cell Therapy
How are monoclonal antibodies used in conjunction with CAR T-cell therapy?
A: By directly lysing cancer cells through the CAR mechanism
B: By preventing immune cells from attacking normal tissues
C: By guiding CAR T-cells to the specific antigens on tumor cells, enhancing their activity
D: By reducing the immune response against the CAR T-cells
Answer: C: By guiding CAR T-cells to the specific antigens on tumor cells, enhancing their activity
209. Monoclonal Antibodies and Drug Resistance
What is a potential mechanism by which cancer cells can develop resistance to monoclonal antibody therapy?
A: By decreasing the number of immune cells in the tumor microenvironment
B: By increasing the number of regulatory T cells
C: By enhancing the production of antibodies against the therapy
D: By downregulating or mutating the antigen targeted by the monoclonal antibody
Answer: D: By downregulating or mutating the antigen targeted by the monoclonal antibody
210. Monoclonal Antibodies Against Infectious Diseases
How are monoclonal antibodies used therapeutically against infectious diseases like COVID-19?
A: By binding to viral proteins and neutralizing the virus, preventing infection
B: By increasing the host’s immune response against the virus
C: By blocking cytokine release syndrome
D: By directly destroying viral particles through ADCC
Answer: A: By binding to viral proteins and neutralizing the virus, preventing infection
211. Thymus and T-Cell Maturation
What is the primary role of the thymus in the immune system?
A: To produce B-cells
B: To filter lymph
C: To facilitate the maturation and differentiation of T-cells
D: To activate neutrophils in response to infection
Answer: C: To facilitate the maturation and differentiation of T-cells
212. Thymic Involution and Immunity
What happens to the thymus during aging, and how does it impact the immune system?
A: It increases in size, enhancing immune function
B: It undergoes involution, reducing T-cell output
C: It produces more B-cells to compensate for declining immunity
D: It begins to produce fewer antibodies
Answer: B: It undergoes involution, reducing T-cell output
213. Positive Selection in the Thymus
During T-cell development, what is the purpose of positive selection in the thymus?
A: To ensure that T-cells can recognize self-MHC molecules
B: To eliminate T-cells that react too strongly to self-antigens
C: To activate B-cells for antibody production
D: To destroy T-cells that fail to bind to antigens
Answer: A: To ensure that T-cells can recognize self-MHC molecules
214. Negative Selection and Autoimmunity Prevention
What is the function of negative selection in the thymus?
A: To increase T-cell receptor diversity
B: To activate T-cells that bind weakly to self-antigens
C: To prevent T-cell apoptosis
D: To eliminate T-cells that strongly react to self-antigens, preventing autoimmunity
Answer: D: To eliminate T-cells that strongly react to self-antigens, preventing autoimmunity
215. Thymic Cortex vs. Medulla in T-Cell Development
Where does positive selection primarily occur during T-cell development in the thymus?
A: Thymic cortex
B: Thymic medulla
C: Bone marrow
D: Lymph nodes
Answer: A: Thymic cortex
216. Role of AIRE in Central Tolerance
What is the role of the autoimmune regulator (AIRE) gene in the thymus?
A: It promotes B-cell maturation in the bone marrow
B: It stimulates cytokine production in mature T-cells
C: It aids in positive selection of T-cells
D: It ensures the presentation of peripheral tissue antigens for negative selection, preventing autoimmunity
Answer: D: It ensures the presentation of peripheral tissue antigens for negative selection, preventing autoimmunity
217. DiGeorge Syndrome and Thymic Development
Which immune defect is associated with DiGeorge syndrome?
A: Overproduction of mature T-cells
B: Thymic hypoplasia, leading to impaired T-cell development
C: Increased B-cell function and antibody production
D: Lack of cytokine production in lymph nodes
Answer: B: Thymic hypoplasia, leading to impaired T-cell development
218. Thymus-Derived Regulatory T-Cells
How do regulatory T-cells (Tregs), which are derived from the thymus, contribute to immune tolerance?
A: By stimulating the production of autoantibodies
B: By enhancing the activation of cytotoxic T-cells
C: By suppressing the activity of self-reactive T-cells
D: By promoting inflammation during infection
Answer: C: By suppressing the activity of self-reactive T-cells
219. Thymic Epithelial Cells and T-Cell Education
What role do thymic epithelial cells play in T-cell development?
A: They act as antigen-presenting cells in peripheral tissues
B: They directly produce cytokines that activate T-cells
C: They secrete antibodies to guide T-cell maturation
D: They present self-antigens to developing T-cells during positive and negative selection
Answer: D: They present self-antigens to developing T-cells during positive and negative selection
220. Thymectomy and Immune Function
What is the expected immune outcome in an adult who undergoes thymectomy (removal of the thymus)?
A: Minimal impact, as the thymus has already produced sufficient mature T-cells
B: Complete loss of immune function
C: Increased susceptibility to bacterial infections
D: Permanent suppression of B-cell production
Answer: A: Minimal impact, as the thymus has already produced sufficient mature T-cells
221. Neutrophil Extracellular Traps (NETs)
What is the primary function of Neutrophil Extracellular Traps (NETs) in the immune response?
A: To facilitate neutrophil migration
B: To enhance antigen presentation
C: To trap and kill pathogens by releasing chromatin structures and antimicrobial proteins
D: To promote phagocytosis by dendritic cells
Answer: C: To trap and kill pathogens by releasing chromatin structures and antimicrobial proteins
222. Phagocytosis Mechanism in Macrophages
Which of the following best describes the mechanism by which macrophages engulf pathogens?
A: Antibody binding stimulates endocytosis
B: Opsonization enhances the recognition and engulfment of pathogens by macrophages
C: Pathogen lysis occurs before phagocytosis
D: Macrophages release toxins to kill pathogens before phagocytosis
Answer: B: Opsonization enhances the recognition and engulfment of pathogens by macrophages
223. Dendritic Cells and Antigen Presentation
What is the primary role of dendritic cells in the immune response?
A: To capture and present antigens to T cells, initiating the adaptive immune response
B: To directly kill pathogens via phagocytosis
C: To release cytokines and initiate inflammation
D: To activate B cells in the lymph nodes
Answer: A: To capture and present antigens to T cells, initiating the adaptive immune response
224. Oxidative Burst in Phagocytes
What role does the oxidative burst play in the function of phagocytes?
A: It helps in antigen presentation
B: It stimulates neutrophil recruitment to the infection site
C: It inhibits the production of inflammatory cytokines
D: It generates reactive oxygen species to kill engulfed pathogens
Answer: D: It generates reactive oxygen species to kill engulfed pathogens
225. Macrophage Polarization
What is the function of M2 macrophages during tissue repair?
A: They promote tissue repair and anti-inflammatory responses
B: They secrete pro-inflammatory cytokines to recruit more immune cells
C: They induce antigen presentation and stimulate T cell activation
D: They release reactive oxygen species to destroy pathogens
Answer: A: They promote tissue repair and anti-inflammatory responses
226. Cross-Presentation by Dendritic Cells
What is cross-presentation in dendritic cells?
A: Presentation of extracellular antigens on MHC class II molecules
B: Transfer of antigens between dendritic cells and neutrophils
C: Presentation of self-antigens to prevent autoimmune responses
D: Presentation of extracellular antigens on MHC class I molecules to activate CD8+ T cells
Answer: D: Presentation of extracellular antigens on MHC class I molecules to activate CD8+ T cells
227. Neutrophil Life Span and Function
What limits the lifespan of neutrophils in peripheral tissues?
A: Rapid depletion of their lysosomal enzymes
B: Their short half-life and rapid apoptosis after pathogen clearance
C: Exhaustion of phagocytic receptors
D: Inability to exit the circulatory system
Answer: B: Their short half-life and rapid apoptosis after pathogen clearance
228. Macrophages and Chronic Inflammation
How do macrophages contribute to chronic inflammation?
A: By phagocytosing pathogens and rapidly resolving inflammation
B: By continuously recruiting neutrophils to the site of infection
C: By persistently secreting pro-inflammatory cytokines in response to unresolved infection
D: By differentiating into neutrophils in response to persistent stimuli
Answer: C: By persistently secreting pro-inflammatory cytokines in response to unresolved infection
229. Role of Dendritic Cells in T Cell Activation
How do dendritic cells ensure effective activation of T cells in lymphoid organs?
A: By migrating to the spleen and directly killing pathogens
B: By secreting antibodies that stimulate T cells
C: By producing chemokines that attract T cells to the infection site
D: By expressing both co-stimulatory molecules and presenting processed antigens to T cells
Answer: D: By expressing both co-stimulatory molecules and presenting processed antigens to T cells
230. Phagosome-Lysosome Fusion in Neutrophils
What is the significance of phagosome-lysosome fusion in neutrophils?
A: It allows the degradation of pathogens by lysosomal enzymes
B: It stimulates dendritic cell migration to the infection site
C: It enhances antigen presentation to B cells
D: It initiates the release of antibodies into the bloodstream
Answer: A: It allows the degradation of pathogens by lysosomal enzymes
231. Role of Interferons in Viral Infection Control
What is the primary role of Type I interferons (IFN-α and IFN-β) during a viral infection?
A: To promote viral replication within host cells
B: To increase the production of antibodies
C: To inhibit viral replication and enhance immune cell activity
D: To suppress the immune response and prevent inflammation
Answer: C: To inhibit viral replication and enhance immune cell activity
232. Cytotoxic T Cells and Viral Clearance
How do cytotoxic T lymphocytes (CTLs) contribute to the clearance of viral infections?
A: By producing antibodies that neutralize the virus
B: By recognizing and destroying virus-infected cells through perforin and granzyme release
C: By presenting viral antigens to helper T cells
D: By inducing apoptosis in uninfected cells
Answer: B: By recognizing and destroying virus-infected cells through perforin and granzyme release
233. Antibody-Mediated Neutralization of Viruses
What is the primary mechanism by which antibodies neutralize viral particles?
A: By binding to viral surface proteins, preventing the virus from entering host cells
B: By directly destroying the viral genome
C: By promoting viral replication within host immune cells
D: By preventing viral transcription
Answer: A: By binding to viral surface proteins, preventing the virus from entering host cells
234. Role of NK Cells in Early Viral Infection
What is the role of natural killer (NK) cells during the early stages of a viral infection?
A: They produce antibodies against the virus
B: They secrete interferon-gamma to activate macrophages
C: They promote viral entry into cells
D: They kill virus-infected cells by detecting the absence of MHC class I molecules
Answer: D: They kill virus-infected cells by detecting the absence of MHC class I molecules
235. Helper T Cells in Viral Infections
How do CD4+ helper T cells aid in the immune response to viral infections?
A: By activating B cells to produce antibodies
B: By directly lysing infected cells
C: By inhibiting the immune response to prevent tissue damage
D: By increasing viral replication within the host
Answer: A: By activating B cells to produce antibodies
236. Viral Evasion of the Immune System
Which strategy do viruses often use to evade detection by the host immune system?
A: Enhancing MHC class I expression
B: Increasing host cell apoptosis
C: Stimulating the production of immune cells
D: Downregulating MHC class I molecules to avoid CTL recognition
Answer: D: Downregulating MHC class I molecules to avoid CTL recognition
237. Role of IFN-γ in Viral Infections
How does interferon-gamma (IFN-γ) contribute to the immune response against viral infections?
A: By directly killing virus-infected cells
B: By activating macrophages and promoting antigen presentation
C: By increasing the rate of viral replication
D: By inhibiting the immune response
Answer: B: By activating macrophages and promoting antigen presentation
238. Memory T Cells and Viral Infections
What role do memory T cells play in response to a recurrent viral infection?
A: They prevent the virus from entering the host cells
B: They increase the production of antibodies
C: They quickly respond to subsequent infections by recognizing viral antigens more rapidly
D: They destroy all infected cells indiscriminately
Answer: C: They quickly respond to subsequent infections by recognizing viral antigens more rapidly
239. Viral Latency and Immune Evasion
How does viral latency contribute to immune evasion?
A: By enhancing the production of viral particles during latency
B: By preventing viral genome replication
C: By exposing viral antigens to the immune system
D: By allowing the virus to persist in host cells without being detected by the immune system
Answer: D: By allowing the virus to persist in host cells without being detected by the immune system
240. Cross-Presentation in Viral Immunity
How does cross-presentation aid in the immune response to viral infections?
A: It allows dendritic cells to present extracellular viral antigens on MHC class I molecules, activating cytotoxic T cells
B: It stimulates B cells to produce neutralizing antibodies
C: It increases the rate of viral replication within infected cells
D: It decreases the production of memory T cells
Answer: A: It allows dendritic cells to present extracellular viral antigens on MHC class I molecules, activating cytotoxic T cells
241. Gut Microbiome and Immune Homeostasis
How does the gut microbiome primarily contribute to immune homeostasis?
A: By enhancing the growth of pathogenic bacteria in the intestines
B: By increasing the permeability of the intestinal barrier
C: By regulating the development and function of immune cells such as T-regulatory cells
D: By directly stimulating the production of antibodies against pathogens
Answer: C: By regulating the development and function of immune cells such as T-regulatory cells
242. Short-Chain Fatty Acids (SCFAs) and Immune Modulation
What is the role of short-chain fatty acids (SCFAs) produced by gut microbes in immune function?
A: They enhance the production of inflammatory cytokines
B: They promote anti-inflammatory responses by supporting T-regulatory cells
C: They increase the permeability of the gut lining
D: They inhibit the growth of beneficial gut bacteria
Answer: B: They promote anti-inflammatory responses by supporting T-regulatory cells
243. Gut-Associated Lymphoid Tissue (GALT)
What is the primary role of gut-associated lymphoid tissue (GALT) in the immune response?
A: To detect antigens in the gut and initiate immune responses
B: To provide nutrients to gut microbiota
C: To produce antibodies against dietary proteins
D: To increase the production of SCFAs in the gut
Answer: A: To detect antigens in the gut and initiate immune responses
244. Microbial Dysbiosis and Disease
How does microbial dysbiosis in the gut contribute to immune-related diseases?
A: By increasing the diversity of the gut microbiome
B: By enhancing the growth of beneficial bacteria
C: By decreasing the permeability of the intestinal barrier
D: By disrupting the balance between pro-inflammatory and anti-inflammatory responses
Answer: D: By disrupting the balance between pro-inflammatory and anti-inflammatory responses
245. Impact of Probiotics on Gut Immunity
How do probiotics influence gut immunity?
A: By promoting the growth of beneficial bacteria and enhancing immune responses
B: By inhibiting the production of SCFAs
C: By increasing the number of pathogenic bacteria
D: By reducing the production of IgA in the gut
Answer: A: By promoting the growth of beneficial bacteria and enhancing immune responses
246. Toll-Like Receptors (TLRs) in the Gut
What role do Toll-like receptors (TLRs) on intestinal epithelial cells play in gut immunity?
A: They directly produce antibodies against gut pathogens
B: They prevent the absorption of dietary antigens
C: They suppress immune responses to maintain tolerance
D: They recognize microbial components and activate immune responses
Answer: D: They recognize microbial components and activate immune responses
247. Impact of Antibiotics on the Gut Microbiome
How can long-term use of antibiotics negatively impact the immune system via the gut microbiome?
A: By increasing the production of SCFAs
B: By reducing microbial diversity and compromising immune regulation
C: By enhancing the growth of beneficial gut bacteria
D: By promoting the secretion of protective mucins in the gut
Answer: B: By reducing microbial diversity and compromising immune regulation
248. Bacteriophages and Immune Modulation
How do bacteriophages in the gut microbiome influence the immune system?
A: By directly competing with host immune cells
B: By increasing gut permeability and allowing pathogen invasion
C: By shaping the composition of bacterial populations, indirectly influencing immune responses
D: By eliminating all bacteria from the gut
Answer: C: By shaping the composition of bacterial populations, indirectly influencing immune responses
249. IgA Production in the Gut
What is the role of secretory IgA in the gut mucosal immunity?
A: It degrades dietary proteins for absorption
B: It enhances the inflammatory response to gut pathogens
C: It prevents bacterial adhesion to the gut epithelium
D: It facilitates the absorption of nutrients in the small intestine
Answer: D: It facilitates the absorption of nutrients in the small intestine
250. Gut Microbiome and Vaccine Responses
How does the gut microbiome influence the efficacy of vaccines?
A: By modulating the immune system's response to antigens introduced by vaccines
B: By increasing gut permeability to improve antigen presentation
C: By directly producing antibodies against vaccine components
D: By eliminating memory T cells after vaccination
Answer: A: By modulating the immune system's response to antigens introduced by vaccines
251. Role of Natural Killer (NK) Cells in Tumor Immunity
How do NK cells primarily recognize and eliminate tumor cells?
A: By detecting tumor-associated antibodies on the cell surface
B: By binding to the major histocompatibility complex (MHC) class I molecules
C: By recognizing the absence or downregulation of MHC class I molecules on tumor cells
D: By identifying tumor cells through complement activation
Answer: C: By recognizing the absence or downregulation of MHC class I molecules on tumor cells
252. Cytotoxic T Cells in Tumor Elimination
What is the primary mechanism by which cytotoxic T cells (CTLs) eliminate tumor cells?
A: By secreting antibodies against tumor antigens
B: By releasing perforin and granzymes to induce apoptosis in target cells
C: By activating NK cells to kill the tumor cells
D: By triggering complement-mediated lysis of tumor cells
Answer: B: By releasing perforin and granzymes to induce apoptosis in target cells
253. Tumor Antigen Presentation
How do dendritic cells (DCs) contribute to anti-tumor immunity?
A: By presenting tumor antigens to T cells, initiating an adaptive immune response
B: By directly attacking tumor cells through phagocytosis
C: By suppressing regulatory T cells that inhibit anti-tumor responses
D: By secreting cytokines that directly destroy tumor cells
Answer: A: By presenting tumor antigens to T cells, initiating an adaptive immune response
254. Tumor Immune Evasion via Checkpoint Molecules
How do cancer cells utilize immune checkpoint molecules to evade immune detection?
A: By upregulating MHC class II molecules
B: By secreting inflammatory cytokines to distract immune cells
C: By inducing the production of antibodies that neutralize T cells
D: By expressing PD-L1, which binds to PD-1 on T cells to inhibit their activity
Answer: D: By expressing PD-L1, which binds to PD-1 on T cells to inhibit their activity
255. Tumor-Specific Antigens
What role do tumor-specific antigens play in the immune response against cancer?
A: They are unique to cancer cells and serve as targets for T cell-mediated destruction
B: They enhance the formation of blood vessels around the tumor
C: They increase tumor cell replication rates
D: They prevent apoptosis in tumor cells
Answer: A: They are unique to cancer cells and serve as targets for T cell-mediated destruction
256. Role of Regulatory T Cells (Tregs) in Tumor Immunity
How do regulatory T cells (Tregs) affect the immune system’s ability to eliminate tumors?
A: By enhancing the cytotoxic activity of NK cells
B: By promoting dendritic cell maturation
C: By increasing the production of tumor-specific antibodies
D: By suppressing anti-tumor immune responses, allowing tumor growth
Answer: D: By suppressing anti-tumor immune responses, allowing tumor growth
257. MHC Class I Downregulation in Tumor Cells
What is the consequence of MHC class I downregulation in tumor cells?
A: It enhances recognition by cytotoxic T cells
B: It reduces recognition by cytotoxic T cells but increases susceptibility to NK cell-mediated killing
C: It protects the tumor from all immune cell recognition
D: It leads to increased tumor cell proliferation
Answer: B: It reduces recognition by cytotoxic T cells but increases susceptibility to NK cell-mediated killing
258. Immunoediting in Cancer Progression
What is the concept of immunoediting in cancer development?
A: The immune system shapes tumor progression by selectively eliminating immunogenic tumor cells
B: The immune system continuously attacks tumor cells, preventing their growth
C: Tumors evolve to evade the immune system by losing immunogenicity over time
D: Tumor cells edit immune cell function to become more aggressive
Answer: C: Tumors evolve to evade the immune system by losing immunogenicity over time
259. Role of Tumor-Associated Macrophages (TAMs) in Cancer
How do tumor-associated macrophages (TAMs) typically contribute to tumor growth and progression?
A: By directly phagocytosing tumor cells
B: By stimulating T cells to attack the tumor
C: By secreting pro-inflammatory cytokines that destroy the tumor
D: By promoting angiogenesis, immune suppression, and tumor cell invasion
Answer: D: By promoting angiogenesis, immune suppression, and tumor cell invasion
260. Checkpoint Inhibitors in Cancer Therapy
How do immune checkpoint inhibitors, such as anti-PD-1 antibodies, enhance anti-tumor immunity?
A: By blocking the interaction between PD-1 on T cells and PD-L1 on tumor cells, restoring T cell activity
B: By increasing the production of tumor-specific antibodies
C: By enhancing the proliferation of regulatory T cells
D: By directly targeting tumor antigens on the cell surface
Answer: A: By blocking the interaction between PD-1 on T cells and PD-L1 on tumor cells, restoring T cell activity
261. Role of Major Histocompatibility Complex (MHC) in Transplant Rejection
How does the difference in MHC between donor and recipient primarily influence transplant rejection?
A: By enhancing T-cell tolerance to the graft
B: By reducing antibody production against the graft
C: By presenting donor antigens that are recognized as foreign by the recipient’s T cells
D: By blocking cytokine release in the recipient
Answer: C: By presenting donor antigens that are recognized as foreign by the recipient’s T cells
262. Hyperacute Rejection Mechanism
What is the primary mechanism involved in hyperacute transplant rejection?
A: T-cell mediated lysis of donor cells
B: Preformed recipient antibodies binding to donor antigens, leading to complement activation
C: Gradual development of donor-specific antibodies over time
D: Tolerance induced by immunosuppressive therapy
Answer: B: Preformed recipient antibodies binding to donor antigens, leading to complement activation
263. Direct Allorecognition in Transplant Rejection
How does direct allorecognition contribute to transplant rejection?
A: Recipient T cells directly recognize donor MHC molecules on graft cells
B: Antibodies from the recipient bind directly to donor cells
C: Donor cells recognize and attack recipient tissues
D: Graft cells secrete cytokines that attract recipient neutrophils
Answer: A: Recipient T cells directly recognize donor MHC molecules on graft cells
264. Chronic Rejection Characteristics
Which of the following best describes chronic transplant rejection?
A: It occurs within minutes of transplantation
B: It is mediated by preformed antibodies
C: It involves acute inflammation and rapid destruction of the graft
D: It is a slow process characterized by fibrosis and loss of graft function over time
Answer: D: It is a slow process characterized by fibrosis and loss of graft function over time
265. Role of Immunosuppressive Drugs
How do immunosuppressive drugs like cyclosporine help in preventing transplant rejection?
A: By inhibiting the activation of T cells that recognize the graft
B: By promoting graft antigen presentation to recipient T cells
C: By enhancing the production of donor-specific antibodies
D: By increasing the activity of natural killer (NK) cells
Answer: A: By inhibiting the activation of T cells that recognize the graft
266. Mechanism of Graft-Versus-Host Disease (GVHD)
What is the primary mechanism of graft-versus-host disease (GVHD) in bone marrow transplants?
A: Recipient immune cells attack the donor graft
B: Donor immune cells attack the recipient’s tissues
C: Recipient antibodies neutralize donor antigens
D: T cells from the donor graft recognize and attack the recipient’s tissues
Answer: D: T cells from the donor graft recognize and attack the recipient’s tissues
267. Indirect Allorecognition Pathway
What is the role of the indirect allorecognition pathway in transplant rejection?
A: Recipient dendritic cells process donor antigens and present them to recipient T cells
B: Recipient B cells directly recognize donor MHC molecules
C: Recipient neutrophils mediate immediate rejection
D: Donor T cells directly attack recipient tissues
Answer: B: Recipient dendritic cells process donor antigens and present them to recipient T cells
268. Crossmatch Test and Transplant Compatibility
What is the purpose of a crossmatch test before organ transplantation?
A: To match the blood types of the donor and recipient
B: To determine the genetic compatibility between donor and recipient
C: To detect preformed antibodies in the recipient that may cause hyperacute rejection
D: To test for infections in the donor organ
Answer: C: To detect preformed antibodies in the recipient that may cause hyperacute rejection
269. Antibody-Mediated Rejection (AMR)
Which mechanism is involved in antibody-mediated rejection (AMR) of transplants?
A: Activation of T cells specific to donor MHC
B: Destruction of the graft by recipient NK cells
C: Secretion of donor antigens into the bloodstream
D: Binding of recipient antibodies to donor endothelial cells, leading to complement activation
Answer: D: Binding of recipient antibodies to donor endothelial cells, leading to complement activation
270. Regulatory T Cells (Tregs) in Transplant Tolerance
How do regulatory T cells (Tregs) contribute to transplant tolerance?
A: By suppressing the activation and proliferation of effector T cells that target the graft
B: By enhancing antigen presentation in the graft
C: By promoting the formation of fibrosis in the graft
D: By stimulating B cells to produce anti-graft antibodies
Answer: A: By suppressing the activation and proliferation of effector T cells that target the graft
271. NK Cell Target Recognition
How do natural killer (NK) cells differentiate between healthy cells and infected or cancerous cells?
A: By recognizing pathogen-associated molecular patterns (PAMPs) on target cells
B: By detecting antibodies bound to target cells via Fc receptors
C: By sensing the absence of MHC class I molecules on target cells
D: By binding to CD4 receptors on target cells
Answer: C: By sensing the absence of MHC class I molecules on target cells
272. Role of Perforin in NK Cell Function
What is the function of perforin in the cytotoxic activity of NK cells?
A: To bind to antigens on the surface of infected cells
B: To create pores in the target cell membrane, allowing granzymes to enter
C: To recruit other immune cells to the site of infection
D: To promote the expression of cytokines in the infected cell
Answer: B: To create pores in the target cell membrane, allowing granzymes to enter
273. Activation of NK Cells by Cytokines
Which cytokine plays a crucial role in the activation and enhancement of NK cell cytotoxicity?
A: Interleukin-2 (IL-2)
B: Interleukin-10 (IL-10)
C: Tumor necrosis factor-alpha (TNF-α)
D: Transforming growth factor-beta (TGF-β)
Answer: A: Interleukin-2 (IL-2)
274. NK Cell-Mediated Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)
Which receptor on NK cells is involved in antibody-dependent cell-mediated cytotoxicity (ADCC)?
A: MHC class II receptor
B: CD28 receptor
C: TLR4 receptor
D: FcγRIII (CD16) receptor
Answer: D: FcγRIII (CD16) receptor
275. Inhibitory Receptors on NK Cells
How do inhibitory receptors on NK cells contribute to self-tolerance?
A: By binding to MHC class I molecules on normal cells, preventing NK cell activation
B: By enhancing the production of cytokines that suppress immune responses
C: By promoting NK cell apoptosis in the presence of self-antigens
D: By releasing granzyme into healthy cells to trigger their death
Answer: A: By binding to MHC class I molecules on normal cells, preventing NK cell activation
276. Granzyme Function in NK Cell Activity
What role do granzymes play in the function of NK cells?
A: They increase the mobility of NK cells in tissues
B: They inhibit the proliferation of infected cells
C: They enhance the expression of MHC class I molecules on infected cells
D: They induce apoptosis in the target cell by cleaving cellular proteins
Answer: D: They induce apoptosis in the target cell by cleaving cellular proteins
277. NK Cells and Interferon Production
Which interferon produced by NK cells enhances their cytotoxic activity and stimulates other immune responses?
A: Interferon-gamma (IFN-γ)
B: Interferon-alpha (IFN-α)
C: Interferon-beta (IFN-β)
D: Interferon-lambda (IFN-λ)
Answer: B: Interferon-alpha (IFN-α)
278. Missing Self Hypothesis
What is the central concept of the "missing self" hypothesis in NK cell function?
A: NK cells recognize and kill cells that lack MHC class I molecules
B: NK cells are activated by the presence of stress ligands on target cells
C: NK cells kill cells that are deficient in self-MHC class I molecules
D: NK cells destroy cells expressing MHC class II molecules
Answer: C: NK cells kill cells that are deficient in self-MHC class I molecules
279. Role of Activating Receptors on NK Cells
What is the role of activating receptors on NK cells?
A: To recognize self-antigens and inhibit cytotoxic activity
B: To increase MHC class I expression on target cells
C: To induce apoptosis in self-cells
D: To bind stress-induced ligands on infected or transformed cells, promoting NK cell activation
Answer: D: To bind stress-induced ligands on infected or transformed cells, promoting NK cell activation
280. NK Cells in Tumor Immunosurveillance
What role do NK cells play in tumor immunosurveillance?
A: They recognize and destroy tumor cells that downregulate MHC class I molecules
B: They prevent angiogenesis in tumors
C: They release cytokines that cause tumor cell proliferation
D: They suppress T-cell activity within the tumor microenvironment
Answer: A: They recognize and destroy tumor cells that downregulate MHC class I molecules
281. Mechanism of Autoimmune Diseases
What is a primary mechanism leading to the development of autoimmune diseases?
A: Decreased production of immune cells
B: Overproduction of cytokines
C: Failure of immune tolerance, resulting in the recognition of self-antigens as foreign
D: Increased number of regulatory T cells
Answer: C: Failure of immune tolerance, resulting in the recognition of self-antigens as foreign
282. Role of Cytokine Storms in Disease
How do cytokine storms contribute to disease progression in infections such as COVID-19?
A: By inhibiting viral replication
B: By causing excessive inflammation and tissue damage due to overactive immune signaling
C: By directly attacking and neutralizing the pathogen
D: By promoting healing and tissue regeneration
Answer: B: By causing excessive inflammation and tissue damage due to overactive immune signaling
283. Type I Hypersensitivity Reactions
What is the initial immune response that leads to a Type I hypersensitivity reaction?
A: Binding of allergens to IgE antibodies on mast cells, triggering degranulation
B: Activation of complement proteins by the antigen
C: Activation of CD8+ T cells to destroy infected cells
D: Production of antibodies that target host tissues
Answer: A: Binding of allergens to IgE antibodies on mast cells, triggering degranulation
284. Role of T Regulatory Cells (Tregs) in Autoimmunity
What is the function of T regulatory cells (Tregs) in preventing autoimmune diseases?
A: By increasing the production of autoantibodies
B: By promoting the differentiation of effector T cells
C: By enhancing the production of pro-inflammatory cytokines
D: By suppressing immune responses that target self-antigens
Answer: D: By suppressing immune responses that target self-antigens
285. Mechanism of Rheumatoid Arthritis
Which immune mechanism is primarily responsible for the progression of rheumatoid arthritis?
A: Production of autoantibodies that target the synovium
B: T cell-mediated destruction of muscle tissue
C: Activation of the complement system leading to lysis of red blood cells
D: IgE-mediated allergic response to environmental antigens
Answer: A: Production of autoantibodies that target the synovium
286. Role of Immune Complexes in Type III Hypersensitivity
How do immune complexes contribute to tissue damage in Type III hypersensitivity reactions?
A: By stimulating T cell proliferation
B: By directly lysing host cells
C: By inhibiting the production of pro-inflammatory cytokines
D: By depositing in tissues, leading to complement activation and inflammation
Answer: D: By depositing in tissues, leading to complement activation and inflammation
287. Molecular Mimicry and Autoimmune Diseases
What role does molecular mimicry play in the development of autoimmune diseases?
A: By allowing immune cells to differentiate between self and non-self
B: By causing cross-reactivity between foreign antigens and self-antigens, leading to an immune attack on self-tissues
C: By enhancing the immune response to pathogenic bacteria
D: By increasing the production of T regulatory cells
Answer: B: By causing cross-reactivity between foreign antigens and self-antigens, leading to an immune attack on self-tissues
288. Mechanism of Immune Surveillance in Cancer
How does immune surveillance prevent the progression of cancer?
A: By increasing the production of cancer-specific antibodies
B: By stimulating angiogenesis to promote immune cell infiltration
C: By recognizing and eliminating cells that express abnormal proteins, such as tumor antigens
D: By suppressing the immune system’s ability to recognize self-antigens
Answer: C: By recognizing and eliminating cells that express abnormal proteins, such as tumor antigens
289. Role of Complement System in Immune-Mediated Diseases
How does the complement system contribute to the pathogenesis of immune-mediated diseases such as lupus?
A: By preventing the activation of the classical pathway
B: By enhancing antibody production against self-antigens
C: By promoting tolerance to foreign antigens
D: By forming membrane attack complexes (MACs) that damage host tissues
Answer: D: By forming membrane attack complexes (MACs) that damage host tissues
290. Mechanism of Graft Rejection
What is the primary mechanism by which the immune system rejects transplanted organs?
A: By recognizing foreign major histocompatibility complex (MHC) molecules on donor cells and initiating a cytotoxic response
B: By producing excessive amounts of immunoglobulins
C: By increasing the number of regulatory T cells
D: By promoting angiogenesis in the transplanted tissue
Answer: A: By recognizing foreign major histocompatibility complex (MHC) molecules on donor cells and initiating a cytotoxic response
291. Role of HLA in Disease Susceptibility
How do variations in human leukocyte antigen (HLA) genes contribute to disease susceptibility?
A: By altering the structure of cytokines
B: By decreasing the body's ability to recognize self-antigens
C: By affecting antigen presentation to T cells, leading to differential immune responses
D: By reducing the overall number of T cells
Answer: C: By affecting antigen presentation to T cells, leading to differential immune responses
292. Genetic Polymorphisms in Autoimmune Diseases
Which type of genetic polymorphism is most commonly associated with autoimmune diseases?
A: Silent mutations in non-coding regions
B: Single nucleotide polymorphisms (SNPs) in immune regulatory genes
C: Structural variations in ribosomal RNA
D: Frameshift mutations in antibody genes
Answer: B: Single nucleotide polymorphisms (SNPs) in immune regulatory genes
293. Impact of Gene-Environment Interactions
What role do gene-environment interactions play in disease susceptibility?
A: Genetic factors influence how the immune system responds to environmental triggers, increasing or decreasing disease risk
B: Environmental factors directly cause genetic mutations leading to disease
C: Gene-environment interactions prevent the development of autoimmune diseases
D: Genetic predispositions are unaffected by environmental influences
Answer: A: Genetic factors influence how the immune system responds to environmental triggers, increasing or decreasing disease risk
294. Epigenetic Modifications and Immune System Regulation
How do epigenetic modifications contribute to immune system regulation?
A: By causing permanent changes in DNA sequences
B: By enhancing the mutation rate in immune cells
C: By increasing the degradation of immune-related proteins
D: By altering gene expression without changing the underlying DNA sequence
Answer: D: By altering gene expression without changing the underlying DNA sequence
295. MHC Polymorphism and Pathogen Resistance
Why is high polymorphism in major histocompatibility complex (MHC) genes advantageous in populations?
A: It increases the ability to recognize a wide variety of pathogens
B: It prevents the development of allergies
C: It decreases the risk of autoimmunity
D: It reduces the likelihood of viral mutations
Answer: A: It increases the ability to recognize a wide variety of pathogens
296. Genetic Basis of Primary Immunodeficiency Diseases
What is the primary cause of most primary immunodeficiency diseases (PIDs)?
A: Environmental factors like chronic infections
B: Somatic mutations in immune cells
C: Overactivation of immune responses
D: Mutations in genes that regulate immune system development or function
Answer: D: Mutations in genes that regulate immune system development or function
297. Genetic Contribution to Asthma Susceptibility
Which genetic component is often linked to an increased risk of developing asthma?
A: Mutations in cytokine genes that regulate inflammatory responses
B: Polymorphisms in genes involved in immune system regulation and airway hyperresponsiveness
C: Mutations in B-cell receptor genes
D: Polymorphisms that affect lipid metabolism
Answer: B: Polymorphisms in genes involved in immune system regulation and airway hyperresponsiveness
298. Gene Editing and Disease Resistance
How can gene editing techniques, such as CRISPR-Cas9, be used to reduce disease susceptibility?
A: By directly altering immune response genes to confer resistance to specific pathogens
B: By deleting non-coding regions of DNA
C: By introducing protective mutations in genes associated with immune regulation
D: By removing polymorphisms linked to autoimmune diseases
Answer: C: By introducing protective mutations in genes associated with immune regulation
299. Influence of Genetic Drift on Immune Variation
How does genetic drift influence immune system variation in populations?
A: It increases immune system uniformity in large populations
B: It decreases the likelihood of pathogen resistance
C: It causes rapid increases in immune gene polymorphisms
D: It can lead to the loss or fixation of immune-related alleles in small populations
Answer: D: It can lead to the loss or fixation of immune-related alleles in small populations
300. Impact of Copy Number Variations (CNVs) in Immunogenetics
What is the significance of copy number variations (CNVs) in the context of immunogenetics?
A: CNVs can lead to variations in immune gene dosage, affecting immune responses and susceptibility to diseases
B: CNVs are unrelated to immune function
C: CNVs decrease the diversity of immune cell receptors
D: CNVs prevent the expression of HLA genes
Answer: A: CNVs can lead to variations in immune gene dosage, affecting immune responses and susceptibility to diseases
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