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Immunology Final Master Study Deck

Comprehensive high-yield deck built from the 12-year past-paper yield analysis + curated study guide. Ordered: proven high-yield core (cross-era + reform champions + sniper list) then the full Chapter 1-6 + Lab Block course flow.

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  1. Front
    Secretory IgA protects mucosal surfaces by which mechanism?
    Back
    Preventing microbial adherence to the mucosa
  2. Front
    Does secretory IgA fix complement?
    Back
    No, sIgA does not fix complement
  3. Front
    What is the structural form of secretory IgA?
    Back
    A dimer joined by a J chain plus secretory component
  4. Front
    What joins the two monomers of secretory IgA?
    Back
    The J chain
  5. Front
    What is the main function of secretory IgA in the oral cavity?
    Back
    Mucosal surveillance, preventing microbial adherence
  6. Front
    Which immunoglobulin carries the secretory component?
    Back
    Secretory IgA
  7. Front
    Which IgA subclass is the preferred key for secretory component?
    Back
    IgA2
  8. Front
    IgE antibody: what is its defining property?
    Back
    It binds strongly to mast cells
  9. Front
    Does IgE fix complement?
    Back
    No
  10. Front
    Which hypersensitivity type does IgE mediate?
    Back
    Type I
  11. Front
    What are the four mechanisms of self-tolerance (autotolerance)?
    Back
    Clonal deletion, clonal anergy, active suppression (Tregs), sequestration of antigens
  12. Front
    Which cells mediate active suppression in self-tolerance?
    Back
    Tregs
  13. Front
    Which cytokines mediate hepatic acute-phase protein release?
    Back
    IL-1 and IL-6
  14. Front
    In the single-answer version, which cytokine is keyed for acute-phase protein release?
    Back
    IL-6
  15. Front
    Contact dermatitis is which type of hypersensitivity?
    Back
    Type IV (delayed-type hypersensitivity, DTH)
  16. Front
    In contact dermatitis (Type IV/DTH), which cells mediate the reaction?
    Back
    Th1 cells and macrophages
  17. Front
    What triggers contact dermatitis at the molecular level?
    Back
    A hapten binding covalently to a skin self-protein, forming a neoantigen
  18. Front
    Metal braces, crowns, and dental fillings may induce which hypersensitivity?
    Back
    Type IV (delayed-type) — contact dermatitis to the metal hapten
  19. Front
    Activation of complement causes tissue damage in which hypersensitivity type?
    Back
    Type III (immune-complex)
  20. Front
    Which cells arrive first in Type III hypersensitivity?
    Back
    Neutrophils
  21. Front
    What mediates the tissue damage in Type III hypersensitivity?
    Back
    Complement
  22. Front
    Give two examples of Type III hypersensitivity reactions.
    Back
    Serum sickness and the Arthus reaction
  23. Front
    Give an example of a privileged immunological site.
    Back
    The testis
  24. Front
    Suppression of Th1 by Th2 is mediated by which cytokine?
    Back
    IL-10
  25. Front
    What advantage does a killed/inactivated vaccine have over live-attenuated?
    Back
    It can be safely given to immunodeficient patients
  26. Front
    Can a live-attenuated vaccine be safely given to an immunodeficient patient?
    Back
    No, it cannot
  27. Front
    In which groups is live-attenuated vaccine contraindicated?
    Back
    Immunodeficiency, pregnancy, and HIV
  28. Front
    Which vaccine type gives the strongest cellular (cell-mediated) immune response?
    Back
    Live-attenuated vaccines
  29. Front
    What are the four mechanisms of autotolerance involve?
    Back
    Clonal deletion, clonal anergy, active suppression (Tregs), sequestration of antigens
  30. Front
    Which tolerance mechanism is broken in atopic (allergic) individuals?
    Back
    Immunological facilitation
  31. Front
    During NK-cell ADCC of a virus-infected cell, what specifically induces the reaction?
    Back
    IgG bound to a viral capsid protein on the target cell's plasma membrane
  32. Front
    Which NK receptor engages the Fc of surface-bound IgG during ADCC?
    Back
    CD16 (FcγR)
  33. Front
    In a secondary CD8 cytotoxic (Tc) response, which cell presents the antigen to the CTL?
    Back
    An MHC class I-expressing somatic (any nucleated) cell
  34. Front
    In a secondary CD8 cytotoxic response, is the presenting cell a professional APC?
    Back
    No - it is the infected somatic cell itself, not a professional APC
  35. Front
    What kind of peptide do effector/memory CD8 CTLs recognize on the target cell?
    Back
    Endogenous peptide on MHC class I
  36. Front
    Tregs enforce clonal anergy through which molecular interaction?
    Back
    Their CTLA-4 (CD152) binds CD80/CD86 (B7) on the APC
  37. Front
    What is the alternative name for CTLA-4?
    Back
    CD152
  38. Front
    How does CTLA-4 remove costimulation from a T cell?
    Back
    It outcompetes CD28 for B7 (CD80/CD86), denying the costimulatory signal
  39. Front
    Does CD28 binding CD80/86 cause anergy or activation?
    Back
    Activation (costimulation), not anergy
  40. Front
    Oxygen-dependent killing by phagocytes is mediated by which agents?
    Back
    Reactive oxygen intermediates (ROIs), nitric oxide (NO), and hypochlorous acid (HOCl)
  41. Front
    What is the role of myeloperoxidase in phagocyte killing?
    Back
    It is the enzyme that makes HOCl (not itself the reactive species)
  42. Front
    A hapten binding to a skin self-protein induces what reaction?
    Back
    Contact hypersensitivity / contact dermatitis
  43. Front
    Contact dermatitis (from a hapten-modified self-protein) is which hypersensitivity type?
    Back
    Type IV (delayed-type hypersensitivity, DTH)
  44. Front
    Which cells mediate contact dermatitis (Type IV / DTH)?
    Back
    Th1 cells and macrophages
  45. Front
    Is hapten-induced contact dermatitis an IgE (Type I) reaction?
    Back
    No - it is Type IV (cell-mediated)
  46. Front
    What antibody causes hemolytic disease of the newborn (HDN)?
    Back
    Incomplete (IgG) anti-D antibodies
  47. Front
    In HDN, what is the maternal Rh status?
    Back
    Rh-negative (and sensitized)
  48. Front
    In HDN, what is the fetal Rh status of the destroyed RBCs?
    Back
    Rh-positive
  49. Front
    Why can the maternal anti-D antibody reach the fetus in HDN?
    Back
    It is IgG, the only class that crosses the placenta
  50. Front
    Must the Rh-negative mother be sensitized for HDN to occur?
    Back
    Yes - she must be previously sensitized to Rh-positive RBCs
  51. Front
    Which infectious disease has been eradicated by vaccination?
    Back
    Smallpox
  52. Front
    Has polio been eradicated by vaccination?
    Back
    No - not yet eradicated
  53. Front
    What is the name of an agent that augments/enhances a vaccine?
    Back
    An adjuvant
  54. Front
    What does an adjuvant do in a vaccine?
    Back
    Augments and prolongs antigen presentation and recruits APCs
  55. Front
    Give an example of a vaccine adjuvant.
    Back
    Alum (aluminum salts)
  56. Front
    What is the defining feature of an antigen-presenting cell (APC)?
    Back
    Expression of MHC class II
  57. Front
    Which cells are the professional APCs?
    Back
    B cells, macrophages, and dendritic cells
  58. Front
    Why is MHC class I not the discriminating marker for APCs?
    Back
    MHC I is on all nucleated cells, so it does not distinguish APCs
  59. Front
    How is information about an antigen's pathogenicity transmitted to T cells?
    Back
    By costimulatory molecules (B7 / CD80/86) on APCs
  60. Front
    What induces APCs to express costimulatory molecules?
    Back
    TLR (PRR) stimulation by PAMPs, signaling danger
  61. Front
    Does the antigen itself (or MHC alone) signal pathogenicity to T cells?
    Back
    No - costimulatory molecules do, after PRR/danger sensing
  62. Front
    What receptor does a naive T cell fail to express that an effector T cell expresses?
    Back
    The high-affinity IL-2 receptor (IL-2R / CD25)
  63. Front
    What is the alternative name for IL-2R alpha chain?
    Back
    CD25
  64. Front
    What is the function of IL-2R / CD25 once expressed on an activated T cell?
    Back
    Drives clonal expansion
  65. Front
    Degradation in proteasomes is characteristic of which class of antigens?
    Back
    Intrinsic (endogenous) antigens
  66. Front
    Proteasomal peptides are loaded onto which MHC class?
    Back
    MHC class I
  67. Front
    Proteasome → MHC I presentation primes which T cell subset?
    Back
    CD8 T cells
  68. Front
    Which processing route do extrinsic/exogenous antigens use?
    Back
    Endosome → MHC class II → CD4 T cells
  69. Front
    Which IgG subclass cannot activate (fix) complement?
    Back
    IgG4
  70. Front
    Which IgG subclasses are the strongest complement fixers?
    Back
    IgG3 > IgG1
  71. Front
    Which complement pathways are strictly innate (antibody-independent)?
    Back
    The alternative and lectin pathways
  72. Front
    Why is the classical complement pathway not strictly innate?
    Back
    It requires antibody to activate
  73. Front
    What does innate immunity recognize?
    Back
    PAMPs (pathogen-associated molecular patterns) and DAMPs (damage-associated molecular patterns)
  74. Front
    Does innate immunity recognize only PAMPs?
    Back
    No - it recognizes both PAMPs and DAMPs
  75. Front
    What causes the vasodilation seen in acute inflammation?
    Back
    Mast-cell degranulation
  76. Front
    Which mediator from mast cells drives early vasodilation in inflammation?
    Back
    Histamine (and other vasoactive mediators)
  77. Front
    Which vaccine type is most effective at inducing a cellular (cell-mediated) immune response?
    Back
    Live-attenuated vaccine
  78. Front
    Why do live-attenuated vaccines give strong cellular immunity?
    Back
    Their replication drives strong CD8/Th1 responses
  79. Front
    Which arm of immunity do killed/inactivated vaccines favor?
    Back
    Humoral immunity
  80. Front
    Activation of CD8 T cells against a weakly pathogenic antigen is supported by which cell?
    Back
    CD4-positive Th1 cells
  81. Front
    How do CD4 Th1 cells help activate CD8 T cells against weak antigens?
    Back
    Via cytokines / dendritic cell licensing
  82. Front
    Which immunoglobulin class is produced by B1 lymphocytes?
    Back
    IgM
  83. Front
    What are the IgM antibodies made by B1 cells described as?
    Back
    Polyreactive natural antibodies, secreted without T-cell help
  84. Front
    Which isotype dominates the early primary immune response?
    Back
    IgM
  85. Front
    Are gingivitis and periodontitis the same disease?
    Back
    No - gingivitis precedes and differs from periodontitis
  86. Front
    What distinguishes periodontitis from gingivitis?
    Back
    Periodontitis involves alveolar bone loss
  87. Front
    What is the keystone pathogen of periodontitis?
    Back
    Porphyromonas gingivalis
  88. Front
    What characterizes severe periodontal disease?
    Back
    Alveolar bone loss
  89. Front
    Which arm(s) of immunity do mRNA COVID-19 vaccines stimulate?
    Back
    Both humoral and cellular
  90. Front
    Why do mRNA COVID-19 vaccines stimulate cellular immunity?
    Back
    Spike is expressed intracellularly → MHC I → CD8/cellular response
  91. Front
    Do mRNA COVID-19 vaccines produce only a humoral response?
    Back
    No - they produce both humoral and cellular responses
  92. Front
    Braces, crowns, and dental fillings may induce which type of hypersensitivity?
    Back
    Delayed-type hypersensitivity (Type IV)
  93. Front
    How do dental metals/materials trigger Type IV hypersensitivity?
    Back
    They act as haptens modifying self-proteins, triggering Th1 + macrophage contact reactions
  94. Front
    What is the best method to define a cell's phenotype (size, granularity, CD markers)?
    Back
    Flow cytometry (FACS)
  95. Front
    In flow cytometry, what does forward scatter measure?
    Back
    Cell size
  96. Front
    In flow cytometry, what does side scatter measure?
    Back
    Granularity
  97. Front
    In flow cytometry, how are CD markers detected?
    Back
    Fluorescent (labeled) antibodies
  98. Front
    What defect does the NBT (nitro-blue tetrazolium) test screen for?
    Back
    Defective intracellular oxidative killing by phagocytes
  99. Front
    A positive (defective) NBT test indicates which disease?
    Back
    Chronic Granulomatous Disease (CGD)
  100. Front
    Why does NBT fail to be reduced in CGD?
    Back
    A failed NADPH-oxidase respiratory burst cannot reduce it
  101. Front
    What immunological event does cross-presentation allow?
    Back
    Activation of a CD8+ T cell by an endocytosed (exogenous) antigen
  102. Front
    In cross-presentation, exogenous antigen is routed onto which MHC class?
    Back
    MHC class I
  103. Front
    Which cells perform cross-presentation?
    Back
    Specialized dendritic cells
  104. Front
    Which cells does HIV infect?
    Back
    CD4+ T-helper cells plus monocytes/macrophages
  105. Front
    What is HIV's primary receptor?
    Back
    CD4
  106. Front
    What are HIV's co-receptors?
    Back
    CXCR4 and CCR5
  107. Front
    Why are monocytes/macrophages HIV targets and reservoirs?
    Back
    They express CD4
  108. Front
    Serum sickness is which type of hypersensitivity?
    Back
    Type III (immune-complex-mediated)
  109. Front
    What is the underlying mechanism of Type III hypersensitivity?
    Back
    Circulating antigen-antibody complexes deposit in tissues
  110. Front
    In Type III hypersensitivity, which cells arrive first?
    Back
    Neutrophils
  111. Front
    What mediates the tissue damage in Type III hypersensitivity?
    Back
    Complement
  112. Front
    Besides serum sickness, name another Type III reaction.
    Back
    The Arthus reaction
  113. Front
    Delayed-type hypersensitivity (DTH) is which type?
    Back
    Type IV
  114. Front
    Which cells mediate Type IV (DTH) hypersensitivity?
    Back
    Th1 cells and macrophages
  115. Front
    Is antibody involved in Type IV (DTH) hypersensitivity?
    Back
    No — it is cell-mediated
  116. Front
    At what time does a DTH reaction peak?
    Back
    48-72 hours
  117. Front
    What is the correct order of steps in a Western blot?
    Back
    Electrophoresis (SDS-PAGE) -> transfer (blotting) -> immunodetection
  118. Front
    In a competitive ELISA, how does absorbance relate to antigen concentration?
    Back
    Inversely (absorbance is proportional to 1/antigen)
  119. Front
    Why is the competitive ELISA relationship inverse?
    Back
    More sample antigen competes off the labeled reagent, lowering signal
  120. Front
    In a sandwich or indirect ELISA, how does absorbance relate to antigen concentration?
    Back
    Directly (more antigen = higher signal)
  121. Front
    Which molecule does a naive T cell fail to express that an effector T cell expresses?
    Back
    IL-2 receptor (CD25)
  122. Front
    When does a T cell acquire the high-affinity IL-2 receptor (CD25)?
    Back
    Upon activation
  123. Front
    Which complement pathways are strictly innate (antibody-independent)?
    Back
    Alternative and lectin pathways
  124. Front
    Which complement pathway requires antibody?
    Back
    The classical pathway
  125. Front
    Which IgG subclass cannot fix complement?
    Back
    IgG4
  126. Front
    Oxygen-dependent killing by phagocytes is mediated by which agents?
    Back
    Reactive oxygen intermediates (ROIs), nitric oxide (NO), and hypochlorous acid (HOCl)
  127. Front
    What does the NBT (or DHR) test screen for?
    Back
    Defective intracellular oxidative (respiratory-burst) killing by phagocytes
  128. Front
    Which disease does an abnormal NBT/DHR test diagnose?
    Back
    Chronic Granulomatous Disease (CGD)
  129. Front
    What is the best method to define a cell's phenotype (size, granularity, CD markers)?
    Back
    Flow cytometry (FACS)
  130. Front
    In flow cytometry, what does forward scatter (FSC) measure?
    Back
    Cell size
  131. Front
    In flow cytometry, what does side scatter (SSC) measure?
    Back
    Cell granularity
  132. Front
    What separation technique does MACS use?
    Back
    Magnetic-bead separation
  133. Front
    In MACS, what does negative selection isolate?
    Back
    The untouched target cells (unwanted cells are labeled and removed)
  134. Front
    What is Ficoll used for?
    Back
    Density-gradient isolation of PBMCs (peripheral blood mononuclear cells)
  135. Front
    In a sandwich or indirect ELISA, how does absorbance relate to antigen concentration?
    Back
    Directly proportional (absorbance increases with antigen)
  136. Front
    In a competitive ELISA, how does absorbance relate to antigen concentration?
    Back
    Inversely proportional (absorbance decreases as antigen increases)
  137. Front
    What is the best test for measuring anti-bacterial serum antibody level?
    Back
    ELISA
  138. Front
    What is the correct order of steps in a Western blot?
    Back
    Electrophoresis -> transfer -> immunodetection
  139. Front
    What does the indirect Coombs test detect?
    Back
    Maternal anti-Rh antibody in the serum (pregnancy screen)
  140. Front
    What does the direct Coombs test detect?
    Back
    Antibody already bound on the RBC surface
  141. Front
    Which vaccine types can be safely given to immunodeficient patients?
    Back
    Killed/inactivated and subunit vaccines
  142. Front
    Can live-attenuated vaccines be given to immunodeficient patients?
    Back
    No - they are contraindicated
  143. Front
    In which patient groups is live-attenuated vaccine contraindicated?
    Back
    Immunodeficiency, pregnancy, and HIV
  144. Front
    Which vaccine type gives the best cell-mediated (cellular) immune response?
    Back
    Live-attenuated vaccines
  145. Front
    Which infectious disease has been eradicated by vaccination?
    Back
    Smallpox
  146. Front
    Which arm(s) of immunity do mRNA COVID-19 vaccines stimulate?
    Back
    Both humoral and cellular
  147. Front
    What does an adjuvant do in a vaccine?
    Back
    Augments and prolongs the antigen's effect / recruits APCs, boosting the immune response
  148. Front
    Give an example of a still-used vaccine adjuvant.
    Back
    Alum
  149. Front
    Which vaccines are the oral polio vaccines?
    Back
    Sabin (oral) and Koprowski
  150. Front
    Is BCG an attenuated vaccine?
    Back
    Yes, BCG is attenuated
  151. Front
    Which vaccines are NOT attenuated (whole-cell pertussis, rabies, HepB candidates)?
    Back
    Pertussis (whole-cell), rabies, and HepB
  152. Front
    Which immunoglobulin class do B1 lymphocytes produce?
    Back
    IgM (natural antibodies)
  153. Front
    Which immunoglobulin class crosses the placenta?
    Back
    IgG only
  154. Front
    Which isotype dominates the early primary immune response?
    Back
    IgM
  155. Front
    Are gingivitis and periodontitis the same condition?
    Back
    No - gingivitis precedes and differs from periodontitis
  156. Front
    What is the keystone pathogen of periodontitis?
    Back
    Porphyromonas gingivalis
  157. Front
    What characterizes severe periodontitis?
    Back
    Alveolar bone loss
  158. Front
    What antibody causes hemolytic disease of the newborn (HDN)?
    Back
    Incomplete (IgG) anti-D antibody
  159. Front
    In HDN, what is the Rh status of the affected mother?
    Back
    Rh-negative and sensitized
  160. Front
    In HDN, what is the Rh status of the affected fetal RBCs that are destroyed?
    Back
    Rh-positive
  161. Front
    Why can the anti-D antibody in HDN reach the fetus?
    Back
    It is IgG, which crosses the placenta
  162. Front
    Which immunoglobulin carries the secretory component?
    Back
    Secretory IgA
  163. Front
    For a 2026 sitting, which IgA subclass is the examiner-preferred key for the secretory component?
    Back
    IgA2
  164. Front
    Which statement about innate immunity recognition is correct?
    Back
    It recognizes both PAMPs and DAMPs
  165. Front
    Does innate immunity have antigen-specific memory?
    Back
    No (it recognizes conserved patterns, not specific antigens)
  166. Front
    What does PAMP stand for?
    Back
    Pathogen-associated molecular pattern
  167. Front
    Give examples of PAMPs.
    Back
    LPS, peptidoglycan, flagellin, dsRNA
  168. Front
    Are PAMPs unique to a single pathogen or shared across microbes?
    Back
    Shared across many different microbes (conserved structures)
  169. Front
    What does DAMP stand for?
    Back
    Damage/danger-associated molecular pattern
  170. Front
    Where do DAMPs come from?
    Back
    Endogenous molecules released by stressed/dying host cells
  171. Front
    How does the diversity of PRRs compare to the TCR?
    Back
    PRRs recognize a limited germline-encoded set; the TCR has far greater clonal diversity
  172. Front
    Are PRRs germline-encoded or clonally rearranged?
    Back
    Germline-encoded
  173. Front
    What is the keyed exam fact about TLR4 and LPS?
    Back
    LPS ligation of TLR4 activates APCs
  174. Front
    Which TLR senses LPS?
    Back
    TLR4
  175. Front
    On which type of bacteria is LPS found?
    Back
    Gram-negative bacteria
  176. Front
    State the TLR4 signaling chain (LPS to APC).
    Back
    LPS → TLR4 → APC activation
  177. Front
    Which inflammasome activates IL-1β?
    Back
    The NLRP3 inflammasome
  178. Front
    What does the NLRP3 inflammasome do to pro-IL-1β?
    Back
    Processes it into active IL-1β
  179. Front
    Which two cytokines drive the hepatic acute-phase protein response?
    Back
    IL-1 and IL-6
  180. Front
    Which cytokine pairs are distractors for the acute-phase response?
    Back
    IL-12+IFN-γ, IL-4+IL-5, TGF-β+IL-10
  181. Front
    In the single-answer phrasing, which ONE cytokine is keyed for acute-phase protein release?
    Back
    IL-6
  182. Front
    What causes the vasodilation seen in acute inflammation?
    Back
    Mast-cell degranulation (releasing histamine/vasoactive mediators)
  183. Front
    Which leukocyte dominates the site during the first ~6 hours of acute inflammation?
    Back
    Neutrophils
  184. Front
    Which cells arrive later than neutrophils in acute inflammation?
    Back
    Macrophages/monocytes
  185. Front
    List the oxygen-dependent (oxidative) killing products of phagocytes.
    Back
    Reactive oxygen intermediates (ROIs), nitric oxide (NO), hypochlorous acid (HOCl)
  186. Front
    In the oxidative-killing item, why is myeloperoxidase a distractor?
    Back
    It is the enzyme that makes HOCl, not a reactive species itself
  187. Front
    Which enzyme generates the superoxide of the respiratory burst in phagocytes?
    Back
    NADPH oxidase
  188. Front
    What does the NBT (nitro-blue tetrazolium) / DHR test screen for?
    Back
    Defective intracellular oxidative (respiratory-burst) killing by phagocytes
  189. Front
    An abnormal NBT/DHR test points to which disease?
    Back
    Chronic Granulomatous Disease (CGD)
  190. Front
    What is the underlying defect in Chronic Granulomatous Disease?
    Back
    Defective NADPH oxidase → failed respiratory burst
  191. Front
    Why does NBT fail to be reduced in CGD?
    Back
    No reactive oxygen species are generated
  192. Front
    Which CD marker is found on ALL T cells?
    Back
    CD3
  193. Front
    What is CD3 part of?
    Back
    The TCR signaling complex
  194. Front
    Which CD marker defines helper T cells?
    Back
    CD4
  195. Front
    On which non-T cells is CD4 also expressed?
    Back
    Monocytes/macrophages
  196. Front
    CD4 is the primary receptor for which virus?
    Back
    HIV
  197. Front
    What are HIV's co-receptors?
    Back
    CXCR4 and CCR5
  198. Front
    Which CD marker defines cytotoxic T cells?
    Back
    CD8
  199. Front
    Cytotoxic (CD8) T cells recognize peptide presented on which MHC class?
    Back
    MHC class I
  200. Front
    Which CD marker is the monocyte/macrophage LPS co-receptor?
    Back
    CD14
  201. Front
    CD14 works with which TLR in LPS sensing?
    Back
    TLR4
  202. Front
    Which CD marker defines B lymphocytes?
    Back
    CD19
  203. Front
    Which CD marker is the defining phenotypic marker of NK cells?
    Back
    CD56
  204. Front
    Which receptor (not CD56) mediates ADCC on NK cells?
    Back
    CD16 (FcγRIII)
  205. Front
    Which CD marker is found on all T cells?
    Back
    CD3
  206. Front
    Which CD marker defines helper T cells?
    Back
    CD4
  207. Front
    Besides helper T cells, which cells also express CD4?
    Back
    Monocytes/macrophages
  208. Front
    CD4 is the primary receptor for which virus?
    Back
    HIV
  209. Front
    Which CD marker defines cytotoxic T cells?
    Back
    CD8
  210. Front
    Which CD marker is the monocyte/macrophage LPS co-receptor?
    Back
    CD14
  211. Front
    Which CD marker defines B lymphocytes?
    Back
    CD19
  212. Front
    Which CD marker defines NK cells?
    Back
    CD56
  213. Front
    Which receptor on NK cells mediates ADCC?
    Back
    CD16 (FcγRIII)
  214. Front
    Name a principal immune function of the macrophage besides phagocytosis.
    Back
    Antigen presentation
  215. Front
    What is efferocytosis, a macrophage function?
    Back
    Clearance of apoptotic cells
  216. Front
    Which professional APC links innate and adaptive immunity via antigen presentation?
    Back
    The macrophage
  217. Front
    Macrophages present antigen on which MHC class?
    Back
    MHC class II
  218. Front
    Name the tissue macrophage of the liver.
    Back
    Kupffer cell
  219. Front
    Name the tissue macrophage of the CNS/brain.
    Back
    Microglia
  220. Front
    Name the bone macrophage-lineage cell that resorbs bone.
    Back
    Osteoclast
  221. Front
    Which cells mediate alveolar bone loss in periodontitis?
    Back
    Osteoclasts
  222. Front
    Which complement pathways are strictly innate (antibody-independent)?
    Back
    Alternative and lectin pathways
  223. Front
    Why is the classical complement pathway not strictly innate?
    Back
    It requires antibody
  224. Front
    What triggers the classical complement pathway?
    Back
    Antigen-antibody complexes (antibody)
  225. Front
    With which component does the classical complement pathway begin?
    Back
    C1
  226. Front
    After C1, which components continue the classical pathway?
    Back
    C4 then C2
  227. Front
    C4 and C2 of the classical pathway form which convertase?
    Back
    The C3 convertase
  228. Front
    Which complement components form the membrane attack complex (MAC)?
    Back
    C5b-C9
  229. Front
    What does the membrane attack complex (C5b-9) do?
    Back
    Forms a lytic pore in the target membrane
  230. Front
    The MAC is the terminal pathway common to how many complement routes?
    Back
    All three
  231. Front
    Which IgG subclass cannot fix the classical complement pathway?
    Back
    IgG4
  232. Front
    Besides IgG4, which immunoglobulin class does not fix the classical pathway?
    Back
    IgA
  233. Front
    Which are the primary (central) lymphoid organs?
    Back
    Thymus and bone marrow
  234. Front
    What defines a primary lymphoid organ?
    Back
    Where lymphocytes develop/mature
  235. Front
    Where do T cells mature?
    Back
    The thymus
  236. Front
    Where do B lymphocytes mature?
    Back
    The bone marrow
  237. Front
    Which adhesion molecules guide lymphocyte homing/extravasation into tissues?
    Back
    Selectins (via rolling)
  238. Front
    Where do dendritic cells primarily present antigen to T cells?
    Back
    The lymph nodes
  239. Front
    Lymph nodes are which category of lymphoid organ?
    Back
    Secondary lymphoid organs
  240. Front
    Which cells directly kill virus-infected cells without prior sensitization?
    Back
    NK (natural killer) cells
  241. Front
    Which cytotoxic molecules do NK cells share with CD8 CTLs?
    Back
    Perforin and granzyme
  242. Front
    Through which receptor do NK cells mediate ADCC?
    Back
    CD16 (FcγRIII)
  243. Front
    In ADCC, what does the NK cell CD16 bind?
    Back
    The Fc of IgG coating the target
  244. Front
    Which cells provide protection against intracellular pathogens?
    Back
    T cells and NK cells
  245. Front
    What type of inflammatory process drives alveolar bone loss in periodontitis?
    Back
    A chronic, cytokine-driven process activating osteoclasts
  246. Front
    Which mediators drive osteoclast activation in periodontitis?
    Back
    IL-1, TNF, IL-6, RANKL
  247. Front
    On 'periodontitis statements except,' which statement is false?
    Back
    That gingivitis and periodontitis are the same
  248. Front
    Which condition precedes periodontitis?
    Back
    Gingivitis
  249. Front
    What is the keystone pathogen of periodontitis?
    Back
    P. gingivalis
  250. Front
    Severe periodontitis is characterized by what tissue change?
    Back
    Alveolar bone loss
  251. Front
    What is the best laboratory method to define a cell's phenotype (size, granularity, CD markers)?
    Back
    Flow cytometry (FACS)
  252. Front
    In flow cytometry, what does forward scatter (FSC) measure?
    Back
    Cell size
  253. Front
    In flow cytometry, what does side scatter (SSC) measure?
    Back
    Granularity
  254. Front
    In flow cytometry, how is CD-marker expression detected?
    Back
    Fluorescent antibodies
  255. Front
    Which region of the antibody molecule binds antigen?
    Back
    The Fab region (fragment antigen-binding)
  256. Front
    Which antibody region mediates complement fixation, placental transfer, ADCC, and cytophilic binding?
    Back
    The Fc region (fragment crystallizable)
  257. Front
    The Fc region is the antibody's effector tail made of which structural part?
    Back
    The constant region
  258. Front
    The constant region of the immunoglobulin heavy chain dictates the antibody's what?
    Back
    Its isotype (antibody class)
  259. Front
    Which antibody property does the heavy-chain constant region determine: isotype, idiotype, or allotype?
    Back
    Isotype
  260. Front
    Which immunoglobulin classes make up the isotypes?
    Back
    IgG, IgA, IgM, IgE, IgD
  261. Front
    What does an antibody's idiotype refer to?
    Back
    Its variable-region/CDR antigen specificity
  262. Front
    What does an antibody's allotype refer to?
    Back
    An allelic (genetic) variant
  263. Front
    What determines antigen-recognition specificity in the variable region of an antibody?
    Back
    The CDRs (complementarity-determining regions / hypervariable loops)
  264. Front
    What part of the antibody do the CDRs form?
    Back
    The antigen-binding paratope
  265. Front
    Another name for the CDRs (complementarity-determining regions)?
    Back
    Hypervariable loops
  266. Front
    What is the function of immunoglobulins (antibodies) in host defense?
    Back
    They tag antigens for destruction and removal
  267. Front
    Antibodies tag antigens, but which components actually do the killing?
    Back
    Complement, phagocytes, and NK cells (ADCC)
  268. Front
    Which single immunoglobulin class crosses the placenta?
    Back
    IgG only
  269. Front
    Placental transfer of IgG is mediated by which antibody region?
    Back
    The Fc region
  270. Front
    What does IgG placental transfer provide to the neonate?
    Back
    Passive neonatal immunity
  271. Front
    What term describes the Fc-mediated ability of antibody to bind immune-cell surfaces (mast cells, macrophages, NK)?
    Back
    Cytophilic binding
  272. Front
    In cytophilic binding, which antibody region adheres to Fc receptors on cells?
    Back
    The Fc region
  273. Front
    In ADCC against a virus-infected cell, what does the NK cell recognize to trigger killing?
    Back
    IgG bound to viral capsid protein on the target cell's plasma membrane
  274. Front
    Which NK receptor binds the Fc of surface-bound IgG during ADCC?
    Back
    CD16 (FcγRIII)
  275. Front
    Secretory IgA protects mucosal surfaces primarily by which mechanism?
    Back
    By preventing microbial adherence to the mucosa
  276. Front
    Does secretory IgA activate complement?
    Back
    No
  277. Front
    What is the molecular form of secretory IgA at mucosal surfaces?
    Back
    A dimer joined by a J chain plus a secretory component
  278. Front
    When is the secretory component added to IgA?
    Back
    During epithelial transcytosis
  279. Front
    What does the secretory component protect IgA from in secretions?
    Back
    Proteolysis
  280. Front
    Which immunoglobulin carries the secretory component and dominates oral-cavity mucosal surveillance?
    Back
    Secretory IgA
  281. Front
    If forced to a subclass, which IgA subclass carries the secretory component (examiner-preferred)?
    Back
    IgA2
  282. Front
    Which immunoglobulin binds strongly to mast cells and mediates Type I hypersensitivity?
    Back
    IgE
  283. Front
    IgE binds which high-affinity receptor on mast cells/basophils?
    Back
    FcεRI
  284. Front
    Does IgE fix (activate) complement?
    Back
    No
  285. Front
    Is IgE abundant in saliva?
    Back
    No
  286. Front
    What is the defining feature of an antigen-presenting cell (APC)?
    Back
    Expression of MHC class II
  287. Front
    Professional APCs present exogenous peptide on MHC II to which T cells?
    Back
    CD4 T cells
  288. Front
    On which cell types is MHC class II found?
    Back
    B cells, dendritic cells (APCs), and macrophages
  289. Front
    Which cells express MHC class I?
    Back
    All nucleated cells
  290. Front
    MHC class I presents endogenous peptide to which T cells?
    Back
    CD8 T cells
  291. Front
    What form of antigen does the T-cell receptor (TCR) recognize?
    Back
    A linear antigenic peptide in the MHC groove
  292. Front
    What form of antigen does the B-cell receptor (BCR) recognize?
    Back
    Soluble, native (conformational) antigen directly
  293. Front
    Are T cells MHC-restricted in their antigen recognition?
    Back
    Yes
  294. Front
    Antigens degraded in the proteasome belong to which processing pathway?
    Back
    Intrinsic (endogenous) antigens
  295. Front
    Proteasome-degraded (endogenous) peptides are loaded onto which MHC class?
    Back
    MHC class I
  296. Front
    Trace the endogenous antigen-processing pathway from degradation to T-cell subset.
    Back
    Proteasome → endogenous antigen → MHC class I → CD8 T cell
  297. Front
    Trace the exogenous antigen-processing pathway from degradation to T-cell subset.
    Back
    Endosome/lysosome → exogenous antigen → MHC class II → CD4 T cell
  298. Front
    What does cross-presentation allow?
    Back
    Activation of a CD8 T cell by endocytosed (exogenous) antigen
  299. Front
    In cross-presentation, exogenous antigen is routed onto which MHC class?
    Back
    MHC class I
  300. Front
    In a secondary CD8 cytotoxic response, which cell presents the antigen?
    Back
    An MHC-I-expressing somatic (any nucleated) cell, not a professional APC
  301. Front
    Which immunoglobulin classes do mature, pre-class-switch (naïve) B cells co-express on their surface?
    Back
    IgM and IgD
  302. Front
    Which immunoglobulin classes do naive (pre-class-switch) B cells co-express on their surface?
    Back
    IgM and IgD
  303. Front
    Which immunoglobulin class is produced by B1 lymphocytes?
    Back
    IgM (natural antibodies)
  304. Front
    What kind of IgM do B1 cells secrete?
    Back
    Low-affinity, polyreactive IgM with little class switching
  305. Front
    Which immunoglobulin isotype dominates the early primary antibody response?
    Back
    IgM
  306. Front
    Which isotypes does class switching produce in the secondary response?
    Back
    IgG, IgA, and IgE
  307. Front
    Which enzymes mediate V(D)J recombination?
    Back
    RAG1 and RAG2 (recombination-activating genes)
  308. Front
    What does V(D)J recombination assemble?
    Back
    The variable region, creating pre-antigen receptor diversity
  309. Front
    By what process does antibody affinity increase during the secondary response?
    Back
    Somatic hypermutation of variable-region genes in germinal centers, then selection
  310. Front
    Where does somatic hypermutation occur?
    Back
    In germinal centers
  311. Front
    Does affinity maturation use RAG/V(D)J recombination?
    Back
    No
  312. Front
    Which IgG subclass is unable to fix complement?
    Back
    IgG4
  313. Front
    Which IgG subclasses are the strong classical-pathway complement fixers?
    Back
    IgG3 and IgG1 (IgG3 strongest)
  314. Front
    Rank IgG1 vs IgG3 for complement-fixing strength.
    Back
    IgG3 > IgG1
  315. Front
    Which IgG subclass is the non-fixer of complement?
    Back
    IgG4
  316. Front
    What does an antibody titer refer to?
    Back
    The highest dilution of serum that still gives a positive result
  317. Front
    Define antibody avidity in terms of affinity and valency.
    Back
    Avidity = affinity × valency (total binding strength)
  318. Front
    What does affinity measure?
    Back
    Single-site binding strength
  319. Front
    Which immunoglobulin is the classic example of high avidity?
    Back
    IgM
  320. Front
    Which helper cell supports CD8 T-cell activation against a weakly-pathogenic antigen?
    Back
    CD4+ Th1 cells
  321. Front
    How do Th1 cells help prime CD8 against low-danger antigens?
    Back
    They license the APC and provide help (IL-2, CD40L)
  322. Front
    What transmits information about an antigen's pathogenicity to T cells?
    Back
    Costimulatory molecules expressed by APCs after TLR stimulation
  323. Front
    Which costimulatory molecules constitute signal 2 to T cells?
    Back
    B7 / CD80-86
  324. Front
    What upregulates B7/CD80-86 on APCs?
    Back
    TLR sensing of PAMPs
  325. Front
    In an antigen-antibody precipitation reaction, what is the physical state of the antigen?
    Back
    Soluble antigen
  326. Front
    What does soluble antigen form when it reacts with antibody in precipitation?
    Back
    An insoluble lattice that precipitates out of solution
  327. Front
    In an agglutination reaction, what is the physical state of the antigen?
    Back
    Particulate antigen
  328. Front
    What happens to particulate antigen when antibody crosslinks it?
    Back
    It clumps (agglutinates)
  329. Front
    Discriminate precipitation vs agglutination by antigen type.
    Back
    Precipitation = soluble antigen lattice; agglutination = particulate antigen clumps
  330. Front
    Blood typing (ABO/Rh) is an example of which antigen-antibody reaction?
    Back
    Agglutination
  331. Front
    Why is blood typing agglutination rather than precipitation?
    Back
    RBCs are particulate antigens
  332. Front
    The latex syphilis test is an example of which antigen-antibody reaction?
    Back
    Agglutination
  333. Front
    Measuring a bacterial titer (clumping of whole bacteria) is which reaction type?
    Back
    Agglutination
  334. Front
    Why is a bacterial titer an agglutination reaction?
    Back
    Whole bacteria are particulate antigens
  335. Front
    What does a high bacterial agglutination titer reflect?
    Back
    A secondary (anamnestic) antibody response
  336. Front
    Name the three classic lab examples of agglutination reactions.
    Back
    Blood typing, latex syphilis test, and bacterial titer
  337. Front
    Which laboratory technique is used to quantify antigen or antibody?
    Back
    Radial immunodiffusion
  338. Front
    In radial immunodiffusion, what is the ring diameter proportional to?
    Back
    Antigen concentration
  339. Front
    What is the primary function of radial immunodiffusion?
    Back
    To quantify antigen or antibody concentration
  340. Front
    What type of method is radial immunodiffusion?
    Back
    A precipitation-in-gel method
  341. Front
    What two principles does immunoelectrophoresis combine?
    Back
    Electrophoretic separation of antigens followed by immunodiffusion
  342. Front
    In immunoelectrophoresis, on what basis are antigens electrophoretically separated?
    Back
    By charge and size
  343. Front
    What forms where separated antigen meets specific antibody in immunoelectrophoresis?
    Back
    Precipitation arcs
  344. Front
    How is antibody titer defined?
    Back
    The highest dilution of serum that still gives a positive result
  345. Front
    A high bacterial agglutination titer indicates which type of immune response?
    Back
    A secondary (anamnestic) response
  346. Front
    Why does a high agglutination titer indicate a secondary response?
    Back
    High antibody levels reflect prior sensitization/memory
  347. Front
    Both precipitation and agglutination depend on which fundamental antibody property?
    Back
    Antibody bivalency/multivalency enabling crosslinking of antigen
  348. Front
    With soluble antigen, antibody crosslinking produces what?
    Back
    A lattice (precipitation)
  349. Front
    With particulate antigen, antibody crosslinking produces what?
    Back
    Clumps (agglutination)
  350. Front
    In a secondary CD8+ cytotoxic response, the antigen is presented on which type of cell?
    Back
    An MHC class I-expressing somatic (any nucleated) cell, not a professional APC
  351. Front
    Which MHC class restricts the cytotoxic CD8+ T-cell secondary effector response?
    Back
    MHC class I
  352. Front
    Which cells express MHC class I (presenting endogenous peptide to CD8 effectors)?
    Back
    All nucleated (somatic) cells
  353. Front
    Why is the secondary CD8 killing target a somatic cell rather than a professional APC?
    Back
    Effector CTLs recognize endogenous peptide on MHC-I of the infected somatic target and kill it directly
  354. Front
    Does the secondary CD8 kill require a professional MHC-II APC?
    Back
    No
  355. Front
    ADCC against a virus-infected cell is induced by which specifically bound molecule?
    Back
    IgG bound to viral capsid protein on the target cell's plasma membrane
  356. Front
    In ADCC, which receptor on the NK cell engages the Fc of the surface-bound IgG?
    Back
    CD16 (FcγRIII)
  357. Front
    In ADCC of a virus-infected cell, where must the antibody-bound antigen be located?
    Back
    On the target cell's plasma membrane (surface)
  358. Front
    Why can't intracellular/cytoplasmic antigen trigger ADCC?
    Back
    It is inaccessible to antibody
  359. Front
    Which antibody isotype mediates ADCC against a virus-infected cell?
    Back
    IgG
  360. Front
    Through which effector receptor does the NK cell engage IgG in ADCC?
    Back
    CD16 (FcγRIII)
  361. Front
    Name the two distinct cytotoxic killing routes used by CTLs and NK cells.
    Back
    Perforin/granzyme (granule-exocytosis) pathway and the FasL-Fas death-receptor pathway
  362. Front
    Besides FasL-Fas, which other receptor pair acts in the death-receptor killing route?
    Back
    TNF-TNFR
  363. Front
    Both CTL/NK killing pathways converge on what fate for the target cell?
    Back
    Apoptosis
  364. Front
    What is the role of perforin in CTL/NK killing?
    Back
    It polymerizes to form pores in the target membrane
  365. Front
    What is the role of granzymes in CTL/NK killing?
    Back
    Serine proteases that enter via perforin pores and trigger the caspase apoptosis cascade
  366. Front
    The perforin/granzyme killing route is also called what?
    Back
    The granule-exocytosis (granule-dependent) route
  367. Front
    Which CTL killing pathway is receptor-dependent rather than granule-dependent?
    Back
    The FasL-Fas (CD95) death-receptor pathway
  368. Front
    In the FasL-Fas pathway, what does CTL FasL engage on the target?
    Back
    Fas (CD95)
  369. Front
    What does Fas engagement on the target trigger?
    Back
    The death-receptor caspase cascade leading to apoptosis
  370. Front
    Do NK cells and CD8+ CTLs share cytotoxic machinery?
    Back
    Yes — both use perforin/granzyme and FasL-Fas
  371. Front
    How does NK recognition differ from CTL recognition?
    Back
    NK killing is MHC-I-independent (missing-self); CTL killing is MHC-I-restricted/antigen-specific
  372. Front
    Which lymphocyte kills virally-infected cells directly without prior sensitization or MHC restriction?
    Back
    NK cells
  373. Front
    By what recognition mechanism do NK cells target cells?
    Back
    Missing-self recognition (innate)
  374. Front
    DTH (delayed-type hypersensitivity) is classified as which hypersensitivity type?
    Back
    Type IV
  375. Front
    DTH is mediated by antibody or by cells?
    Back
    Cell-mediated (T-cell), not antibody
  376. Front
    What is the time course of a delayed-type hypersensitivity reaction?
    Back
    Delayed, 24-72 hours
  377. Front
    Which cells mediate DTH / Type IV hypersensitivity?
    Back
    Th1 cells + macrophages
  378. Front
    How do Th1 cells recruit and activate macrophages in DTH?
    Back
    By releasing IFN-γ
  379. Front
    What is the molecular trigger of allergic contact dermatitis?
    Back
    A hapten binding a skin self-protein (carrier) to form a complete immunogen
  380. Front
    Allergic contact dermatitis is which hypersensitivity type and T-cell subset?
    Back
    Type IV (DTH), Th1-mediated
  381. Front
    Metal braces, crowns, and dental fillings may induce which immune reaction?
    Back
    Delayed-type hypersensitivity (DTH / Type IV)
  382. Front
    How do metal ions in dental materials trigger DTH?
    Back
    They act as haptens binding oral/skin self-proteins, driving a Th1 + macrophage contact reaction
  383. Front
    Contact dermatitis is which hypersensitivity type?
    Back
    Type IV (DTH)
  384. Front
    Contact dermatitis is mediated by which T helper subset?
    Back
    Th1 (with macrophages as effectors)
  385. Front
    Which cytokines drive naïve CD4+ T-cell differentiation toward Th1?
    Back
    IL-12 (from APCs/macrophages) and IFN-γ
  386. Front
    Which transcription factor commits CD4+ T cells to the Th1 lineage?
    Back
    T-bet
  387. Front
    Th1 differentiation supports which type of immunity?
    Back
    Cell-mediated immunity
  388. Front
    Which cytokine drives naïve CD4+ T-cell differentiation toward Th2?
    Back
    IL-4
  389. Front
    Which transcription factor commits CD4+ T cells to the Th2 lineage?
    Back
    GATA3
  390. Front
    Th2 differentiation supports which type of responses?
    Back
    Humoral/allergic responses
  391. Front
    Suppression of Th1 by Th2 is mediated by which cytokine?
    Back
    IL-10
  392. Front
    What is the cellular source of the IL-10 that suppresses Th1?
    Back
    Th2 cells
  393. Front
    Which Th1 cytokine cross-regulates (suppresses) Th2?
    Back
    IFN-gamma
  394. Front
    Which Th2-derived cytokine suppresses Th1?
    Back
    IL-10
  395. Front
    What is the result of the mutual Th1/Th2 cross-regulation called?
    Back
    Immune deviation
  396. Front
    Is CD8+ cytotoxic killing of virally-infected cells a Th1 or Th2 function?
    Back
    Th1 (cell-mediated)
  397. Front
    Which arm of immunity does a Th2 response drive?
    Back
    Humoral / IgE / eosinophil responses
  398. Front
    Which CD4+ T-cell subset recruits and activates macrophages (phagocytes)?
    Back
    Th1
  399. Front
    Which cytokines does Th1 secrete to recruit/activate macrophages?
    Back
    IFN-gamma and IL-2
  400. Front
    What is the principal macrophage-activating signal from Th1 cells?
    Back
    IFN-gamma
  401. Front
    What does IFN-gamma do to macrophages?
    Back
    Activates them, enhancing microbicidal/oxidative killing
  402. Front
    What is the primary autocrine T-cell growth/proliferation cytokine from activated Th1 cells?
    Back
    IL-2
  403. Front
    What does IL-2 do for T cells?
    Back
    Drives clonal proliferation of activated T cells
  404. Front
    Which receptor marks activated/effector T cells (not naive T cells)?
    Back
    IL-2R (CD25)
  405. Front
    Activation of a CD8+ T cell against a weakly-pathogenic antigen is supported by which helper cell?
    Back
    CD4+ Th1
  406. Front
    Why does CD8 activation by a weak antigen require Th1 help?
    Back
    Weak antigens cannot fully license the APC alone
  407. Front
    What does CD4+ Th1 provide to enable CD8 priming against weak antigens?
    Back
    IL-2 and CD40L-mediated APC licensing/costimulation
  408. Front
    Which Th subset orchestrates immunity to intracellular pathogens?
    Back
    Th1
  409. Front
    What cytokines drive Th1 differentiation?
    Back
    IL-12 and IFN-gamma
  410. Front
    How does Th1 fight intracellular microbes?
    Back
    Activates macrophages and supports CD8 CTLs
  411. Front
    Which Th subset handles extracellular/parasitic/allergic responses?
    Back
    Th2
  412. Front
    How does NK cell killing recognize targets (relative to MHC-I)?
    Back
    MHC-I-independent 'missing-self' (kills cells that down-regulate MHC-I)
  413. Front
    How does CD8 CTL killing recognize targets (relative to MHC-I)?
    Back
    MHC-I-restricted, antigen-specific (kills cells presenting peptide on MHC-I)
  414. Front
    What effector machinery do NK cells and CD8 CTLs share?
    Back
    Perforin/granzyme and Fas
  415. Front
    Serum sickness and Arthus reactions are which hypersensitivity type?
    Back
    Type III (immune-complex)
  416. Front
    Delayed-type hypersensitivity (DTH) is which hypersensitivity type?
    Back
    Type IV (cell-mediated)
  417. Front
    Which cells mediate Type IV DTH?
    Back
    Th1 + macrophages
  418. Front
    What are the four mechanisms of autotolerance (self-tolerance)?
    Back
    Clonal deletion, clonal anergy, active suppression (Tregs), sequestration of antigens
  419. Front
    Is 'immune paralysis' one of the four keyed autotolerance mechanisms?
    Back
    No
  420. Front
    Is 'exhaustion of memory cells/clones' one of the four keyed autotolerance mechanisms?
    Back
    No
  421. Front
    Is 'positive/negative selection' the keyed answer for the four mechanisms of autotolerance?
    Back
    No
  422. Front
    What does immunological paralysis refer to?
    Back
    Subliminal-threshold unresponsiveness
  423. Front
    Which tolerance mechanism is broken in atopic (allergic) individuals?
    Back
    Immunological facilitation
  424. Front
    How do Tregs enforce/support clonal anergy (molecular mechanism)?
    Back
    Their CTLA-4 (CD152) binds CD80/CD86 (B7) on the APC
  425. Front
    By binding B7, what does Treg CTLA-4 outcompete?
    Back
    CD28 costimulation
  426. Front
    What is the CD designation for CTLA-4?
    Back
    CD152
  427. Front
    Which APC ligands does Treg CTLA-4 (CD152) bind to enforce anergy?
    Back
    CD80 and CD86 (the B7 molecules)
  428. Front
    What is the CD designation for CTLA-4?
    Back
    CD152
  429. Front
    On the APC, which molecules does CTLA-4 (CD152) bind?
    Back
    CD80/86 (B7)
  430. Front
    What does Treg CTLA-4 (CD152) enforce by binding the APC?
    Back
    Clonal anergy
  431. Front
    Which ligands on the APC does Treg CTLA-4 bind to enforce anergy?
    Back
    CD80 and CD86 (the B7 molecules)
  432. Front
    What is the alternative name for the B7 molecules?
    Back
    CD80 and CD86
  433. Front
    Tregs support clonal anergy by binding what on the APC?
    Back
    CD80/86 (B7)
  434. Front
    Tregs bind CD80/86 on the APC using which of their molecules?
    Back
    CD152 (CTLA-4)
  435. Front
    What two-signal event defines clonal anergy at the T-cell level?
    Back
    Signal 1 (TCR-peptide/MHC) without signal 2 (costimulation)
  436. Front
    What provides signal 2 (costimulation) for T-cell activation?
    Back
    CD28 binding CD80/86
  437. Front
    A naive T cell gets signal 1 but no costimulation - what is the outcome?
    Back
    Clonal anergy (functional unresponsiveness)
  438. Front
    Where does central tolerance occur?
    Back
    Primary lymphoid organs (thymus for T cells, bone marrow for B cells)
  439. Front
    How is central tolerance generated for T cells?
    Back
    Negative selection in the thymus
  440. Front
    In thymic negative selection, which T-cell clones are deleted?
    Back
    Those binding self-peptide on self-MHC too strongly
  441. Front
    Thymic negative selection is an example of which tolerance mechanism?
    Back
    Clonal deletion
  442. Front
    Where are self-reactive B cells deleted during central tolerance?
    Back
    Bone marrow
  443. Front
    Where is peripheral tolerance maintained?
    Back
    Outside the primary lymphoid organs
  444. Front
    Which clones does peripheral tolerance act on?
    Back
    Self-reactive clones that escaped central deletion
  445. Front
    Name the three mechanisms of peripheral tolerance.
    Back
    Clonal anergy, Treg active suppression, antigen sequestration
  446. Front
    Which tolerance mechanisms are central (thymus/bone marrow)?
    Back
    Clonal deletion (negative selection)
  447. Front
    Which tolerance mechanisms are peripheral?
    Back
    Clonal anergy, Treg active suppression, antigen sequestration
  448. Front
    What is the classic example of an immunologically privileged site?
    Back
    The testis
  449. Front
    What is an immunologically privileged site?
    Back
    An anatomical site sequestered from immune surveillance
  450. Front
    Which tolerance mechanism do privileged sites represent?
    Back
    Antigen sequestration
  451. Front
    Define immune ignorance as a tolerance state.
    Back
    Self-reactive lymphocytes coexist with self-antigen but do not respond
  452. Front
    Why does a clone ignore its self-antigen in immune ignorance?
    Back
    Antigen is below the concentration/location threshold to trigger activation
  453. Front
    Define immunological paralysis.
    Back
    Unresponsiveness produced by antigen at a subliminal threshold (e.g., very high/persistent dose)
  454. Front
    Is immunological paralysis the same as anergy?
    Back
    No - it is a distinct term
  455. Front
    Is immunological paralysis part of the four-part autotolerance list?
    Back
    No
  456. Front
    Is immunological paralysis a recognized peripheral-tolerance term?
    Back
    Yes (subliminal-threshold unresponsiveness)
  457. Front
    Define the anamnestic response.
    Back
    The faster, stronger immune response on re-exposure to a previously encountered antigen
  458. Front
    Which cells mediate the anamnestic response?
    Back
    Memory lymphocytes
  459. Front
    Name the two principal mechanisms by which autoimmunity arises.
    Back
    Molecular mimicry and release of sequestered antigens
  460. Front
    What is molecular mimicry as an autoimmunity mechanism?
    Back
    A microbial antigen resembles a self-antigen, so the anti-microbial response cross-reacts with self
  461. Front
    How does release of sequestered antigen cause autoimmunity?
    Back
    Trauma/infection exposes hidden self-antigens the immune system never became tolerant to
  462. Front
    Give examples of privileged sites whose antigen release can trigger autoimmunity.
    Back
    Testis, eye, brain
  463. Front
    Which immunoglobulin is associated with self-reactivity (natural autoantibodies)?
    Back
    Self-reactive IgM
  464. Front
    Active suppression as an autotolerance mechanism is carried out by which cells?
    Back
    Tregs (regulatory T cells)
  465. Front
    Where are self-reactive T cells deleted by clonal deletion?
    Back
    The thymus (negative selection)
  466. Front
    Where are self-reactive B cells deleted by clonal deletion?
    Back
    The bone marrow
  467. Front
    What is clonal deletion?
    Back
    Physical removal of self-reactive clones (central tolerance)
  468. Front
    In clonal deletion, what happens to the self-reactive clone?
    Back
    It is physically removed/killed
  469. Front
    In clonal anergy, what happens to the self-reactive clone?
    Back
    It survives but is rendered functionally unresponsive
  470. Front
    Clonal anergy results from which signaling pattern?
    Back
    Signal 1 without signal 2
  471. Front
    What reinforces clonal anergy beyond signal 1 without signal 2?
    Back
    Treg CTLA-4
  472. Front
    How many classes of hypersensitivity reactions are there?
    Back
    Four (Types I-IV)
  473. Front
    Type I hypersensitivity: principal antibody?
    Back
    IgE
  474. Front
    Type I hypersensitivity: principal effector cell?
    Back
    Mast cells (and basophils)
  475. Front
    Type I hypersensitivity is also called what?
    Back
    Immediate (anaphylactic/atopic) hypersensitivity
  476. Front
    What is the timing of Type I hypersensitivity?
    Back
    Within minutes of re-exposure
  477. Front
    What triggers the Type I reaction at the cellular level?
    Back
    IgE-triggered mast-cell degranulation
  478. Front
    Give two classic clinical examples of Type I hypersensitivity.
    Back
    Atopic dermatitis and anaphylaxis
  479. Front
    Atopic dermatitis is which hypersensitivity type?
    Back
    Type I (IgE/mast-cell mediated)
  480. Front
    Contact dermatitis vs atopic dermatitis: which is Type IV?
    Back
    Contact dermatitis (atopic dermatitis is Type I)
  481. Front
    What triggers mast-cell mediator release in Type I hypersensitivity?
    Back
    Allergen cross-linking IgE bound to mast-cell FcεRI receptors
  482. Front
    What mediators are released on mast-cell degranulation in Type I?
    Back
    Histamine and other mediators
  483. Front
    IgE antibody: what is its defining property?
    Back
    Binds strongly to mast cells
  484. Front
    Does IgE fix complement?
    Back
    No
  485. Front
    Is IgE abundant in saliva?
    Back
    No
  486. Front
    IgE mediates which hypersensitivity type (Type I or IV)?
    Back
    Type I
  487. Front
    Besides allergy, what immune defense is the IgE/mast-cell axis tied to?
    Back
    Anti-helminth (parasite) defense
  488. Front
    Which cell type joins IgE and mast cells in anti-parasite defense?
    Back
    Eosinophils
  489. Front
    Which tolerance mechanism is broken in atopic (allergic) individuals?
    Back
    Immunological facilitation
  490. Front
    Type II hypersensitivity: what is the target of the antibody?
    Back
    An antigen ON a cell or tissue (cell-surface/matrix antigen)
  491. Front
    Type II vs Type III: which involves antibody against a cell-bound antigen?
    Back
    Type II (Type III is against soluble antigen)
  492. Front
    Type II hypersensitivity: what are the main effector mechanisms of damage?
    Back
    Complement activation, phagocytes (opsonization), and ADCC
  493. Front
    Name two classic clinical examples of Type II hypersensitivity.
    Back
    Hemolytic disease of the newborn (HDN) and transfusion reactions
  494. Front
    Transfusion reactions are which hypersensitivity type?
    Back
    Type II
  495. Front
    Why are transfusion reactions Type II?
    Back
    Anti-A/anti-B antibody binds antigens on transfused RBC surface
  496. Front
    What destroys the RBCs in a transfusion reaction?
    Back
    Complement-mediated lysis and phagocytic clearance
  497. Front
    Type III hypersensitivity: what is the causative immune structure?
    Back
    Immune complexes (antibody bound to soluble antigen)
  498. Front
    In Type III hypersensitivity, what kind of antigen does antibody bind?
    Back
    Soluble antigen
  499. Front
    In Type III hypersensitivity, which cells arrive first at the site?
    Back
    Neutrophils (PMNs)
  500. Front
    In Type III, how is tissue damage actually produced?
    Back
    Deposited immune complexes activate complement, attracting neutrophils whose enzymes damage tissue

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