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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- FrontSecretory IgA protects mucosal surfaces by which mechanism?BackPreventing microbial adherence to the mucosa
- FrontDoes secretory IgA fix complement?BackNo, sIgA does not fix complement
- FrontWhat is the structural form of secretory IgA?BackA dimer joined by a J chain plus secretory component
- FrontWhat joins the two monomers of secretory IgA?BackThe J chain
- FrontWhat is the main function of secretory IgA in the oral cavity?BackMucosal surveillance, preventing microbial adherence
- FrontWhich immunoglobulin carries the secretory component?BackSecretory IgA
- FrontWhich IgA subclass is the preferred key for secretory component?BackIgA2
- FrontIgE antibody: what is its defining property?BackIt binds strongly to mast cells
- FrontDoes IgE fix complement?BackNo
- FrontWhich hypersensitivity type does IgE mediate?BackType I
- FrontWhat are the four mechanisms of self-tolerance (autotolerance)?BackClonal deletion, clonal anergy, active suppression (Tregs), sequestration of antigens
- FrontWhich cells mediate active suppression in self-tolerance?BackTregs
- FrontWhich cytokines mediate hepatic acute-phase protein release?BackIL-1 and IL-6
- FrontIn the single-answer version, which cytokine is keyed for acute-phase protein release?BackIL-6
- FrontContact dermatitis is which type of hypersensitivity?BackType IV (delayed-type hypersensitivity, DTH)
- FrontIn contact dermatitis (Type IV/DTH), which cells mediate the reaction?BackTh1 cells and macrophages
- FrontWhat triggers contact dermatitis at the molecular level?BackA hapten binding covalently to a skin self-protein, forming a neoantigen
- FrontMetal braces, crowns, and dental fillings may induce which hypersensitivity?BackType IV (delayed-type) — contact dermatitis to the metal hapten
- FrontActivation of complement causes tissue damage in which hypersensitivity type?BackType III (immune-complex)
- FrontWhich cells arrive first in Type III hypersensitivity?BackNeutrophils
- FrontWhat mediates the tissue damage in Type III hypersensitivity?BackComplement
- FrontGive two examples of Type III hypersensitivity reactions.BackSerum sickness and the Arthus reaction
- FrontGive an example of a privileged immunological site.BackThe testis
- FrontSuppression of Th1 by Th2 is mediated by which cytokine?BackIL-10
- FrontWhat advantage does a killed/inactivated vaccine have over live-attenuated?BackIt can be safely given to immunodeficient patients
- FrontCan a live-attenuated vaccine be safely given to an immunodeficient patient?BackNo, it cannot
- FrontIn which groups is live-attenuated vaccine contraindicated?BackImmunodeficiency, pregnancy, and HIV
- FrontWhich vaccine type gives the strongest cellular (cell-mediated) immune response?BackLive-attenuated vaccines
- FrontWhat are the four mechanisms of autotolerance involve?BackClonal deletion, clonal anergy, active suppression (Tregs), sequestration of antigens
- FrontWhich tolerance mechanism is broken in atopic (allergic) individuals?BackImmunological facilitation
- FrontDuring NK-cell ADCC of a virus-infected cell, what specifically induces the reaction?BackIgG bound to a viral capsid protein on the target cell's plasma membrane
- FrontWhich NK receptor engages the Fc of surface-bound IgG during ADCC?BackCD16 (FcγR)
- FrontIn a secondary CD8 cytotoxic (Tc) response, which cell presents the antigen to the CTL?BackAn MHC class I-expressing somatic (any nucleated) cell
- FrontIn a secondary CD8 cytotoxic response, is the presenting cell a professional APC?BackNo - it is the infected somatic cell itself, not a professional APC
- FrontWhat kind of peptide do effector/memory CD8 CTLs recognize on the target cell?BackEndogenous peptide on MHC class I
- FrontTregs enforce clonal anergy through which molecular interaction?BackTheir CTLA-4 (CD152) binds CD80/CD86 (B7) on the APC
- FrontWhat is the alternative name for CTLA-4?BackCD152
- FrontHow does CTLA-4 remove costimulation from a T cell?BackIt outcompetes CD28 for B7 (CD80/CD86), denying the costimulatory signal
- FrontDoes CD28 binding CD80/86 cause anergy or activation?BackActivation (costimulation), not anergy
- FrontOxygen-dependent killing by phagocytes is mediated by which agents?BackReactive oxygen intermediates (ROIs), nitric oxide (NO), and hypochlorous acid (HOCl)
- FrontWhat is the role of myeloperoxidase in phagocyte killing?BackIt is the enzyme that makes HOCl (not itself the reactive species)
- FrontA hapten binding to a skin self-protein induces what reaction?BackContact hypersensitivity / contact dermatitis
- FrontContact dermatitis (from a hapten-modified self-protein) is which hypersensitivity type?BackType IV (delayed-type hypersensitivity, DTH)
- FrontWhich cells mediate contact dermatitis (Type IV / DTH)?BackTh1 cells and macrophages
- FrontIs hapten-induced contact dermatitis an IgE (Type I) reaction?BackNo - it is Type IV (cell-mediated)
- FrontWhat antibody causes hemolytic disease of the newborn (HDN)?BackIncomplete (IgG) anti-D antibodies
- FrontIn HDN, what is the maternal Rh status?BackRh-negative (and sensitized)
- FrontIn HDN, what is the fetal Rh status of the destroyed RBCs?BackRh-positive
- FrontWhy can the maternal anti-D antibody reach the fetus in HDN?BackIt is IgG, the only class that crosses the placenta
- FrontMust the Rh-negative mother be sensitized for HDN to occur?BackYes - she must be previously sensitized to Rh-positive RBCs
- FrontWhich infectious disease has been eradicated by vaccination?BackSmallpox
- FrontHas polio been eradicated by vaccination?BackNo - not yet eradicated
- FrontWhat is the name of an agent that augments/enhances a vaccine?BackAn adjuvant
- FrontWhat does an adjuvant do in a vaccine?BackAugments and prolongs antigen presentation and recruits APCs
- FrontGive an example of a vaccine adjuvant.BackAlum (aluminum salts)
- FrontWhat is the defining feature of an antigen-presenting cell (APC)?BackExpression of MHC class II
- FrontWhich cells are the professional APCs?BackB cells, macrophages, and dendritic cells
- FrontWhy is MHC class I not the discriminating marker for APCs?BackMHC I is on all nucleated cells, so it does not distinguish APCs
- FrontHow is information about an antigen's pathogenicity transmitted to T cells?BackBy costimulatory molecules (B7 / CD80/86) on APCs
- FrontWhat induces APCs to express costimulatory molecules?BackTLR (PRR) stimulation by PAMPs, signaling danger
- FrontDoes the antigen itself (or MHC alone) signal pathogenicity to T cells?BackNo - costimulatory molecules do, after PRR/danger sensing
- FrontWhat receptor does a naive T cell fail to express that an effector T cell expresses?BackThe high-affinity IL-2 receptor (IL-2R / CD25)
- FrontWhat is the alternative name for IL-2R alpha chain?BackCD25
- FrontWhat is the function of IL-2R / CD25 once expressed on an activated T cell?BackDrives clonal expansion
- FrontDegradation in proteasomes is characteristic of which class of antigens?BackIntrinsic (endogenous) antigens
- FrontProteasomal peptides are loaded onto which MHC class?BackMHC class I
- FrontProteasome → MHC I presentation primes which T cell subset?BackCD8 T cells
- FrontWhich processing route do extrinsic/exogenous antigens use?BackEndosome → MHC class II → CD4 T cells
- FrontWhich IgG subclass cannot activate (fix) complement?BackIgG4
- FrontWhich IgG subclasses are the strongest complement fixers?BackIgG3 > IgG1
- FrontWhich complement pathways are strictly innate (antibody-independent)?BackThe alternative and lectin pathways
- FrontWhy is the classical complement pathway not strictly innate?BackIt requires antibody to activate
- FrontWhat does innate immunity recognize?BackPAMPs (pathogen-associated molecular patterns) and DAMPs (damage-associated molecular patterns)
- FrontDoes innate immunity recognize only PAMPs?BackNo - it recognizes both PAMPs and DAMPs
- FrontWhat causes the vasodilation seen in acute inflammation?BackMast-cell degranulation
- FrontWhich mediator from mast cells drives early vasodilation in inflammation?BackHistamine (and other vasoactive mediators)
- FrontWhich vaccine type is most effective at inducing a cellular (cell-mediated) immune response?BackLive-attenuated vaccine
- FrontWhy do live-attenuated vaccines give strong cellular immunity?BackTheir replication drives strong CD8/Th1 responses
- FrontWhich arm of immunity do killed/inactivated vaccines favor?BackHumoral immunity
- FrontActivation of CD8 T cells against a weakly pathogenic antigen is supported by which cell?BackCD4-positive Th1 cells
- FrontHow do CD4 Th1 cells help activate CD8 T cells against weak antigens?BackVia cytokines / dendritic cell licensing
- FrontWhich immunoglobulin class is produced by B1 lymphocytes?BackIgM
- FrontWhat are the IgM antibodies made by B1 cells described as?BackPolyreactive natural antibodies, secreted without T-cell help
- FrontWhich isotype dominates the early primary immune response?BackIgM
- FrontAre gingivitis and periodontitis the same disease?BackNo - gingivitis precedes and differs from periodontitis
- FrontWhat distinguishes periodontitis from gingivitis?BackPeriodontitis involves alveolar bone loss
- FrontWhat is the keystone pathogen of periodontitis?BackPorphyromonas gingivalis
- FrontWhat characterizes severe periodontal disease?BackAlveolar bone loss
- FrontWhich arm(s) of immunity do mRNA COVID-19 vaccines stimulate?BackBoth humoral and cellular
- FrontWhy do mRNA COVID-19 vaccines stimulate cellular immunity?BackSpike is expressed intracellularly → MHC I → CD8/cellular response
- FrontDo mRNA COVID-19 vaccines produce only a humoral response?BackNo - they produce both humoral and cellular responses
- FrontBraces, crowns, and dental fillings may induce which type of hypersensitivity?BackDelayed-type hypersensitivity (Type IV)
- FrontHow do dental metals/materials trigger Type IV hypersensitivity?BackThey act as haptens modifying self-proteins, triggering Th1 + macrophage contact reactions
- FrontWhat is the best method to define a cell's phenotype (size, granularity, CD markers)?BackFlow cytometry (FACS)
- FrontIn flow cytometry, what does forward scatter measure?BackCell size
- FrontIn flow cytometry, what does side scatter measure?BackGranularity
- FrontIn flow cytometry, how are CD markers detected?BackFluorescent (labeled) antibodies
- FrontWhat defect does the NBT (nitro-blue tetrazolium) test screen for?BackDefective intracellular oxidative killing by phagocytes
- FrontA positive (defective) NBT test indicates which disease?BackChronic Granulomatous Disease (CGD)
- FrontWhy does NBT fail to be reduced in CGD?BackA failed NADPH-oxidase respiratory burst cannot reduce it
- FrontWhat immunological event does cross-presentation allow?BackActivation of a CD8+ T cell by an endocytosed (exogenous) antigen
- FrontIn cross-presentation, exogenous antigen is routed onto which MHC class?BackMHC class I
- FrontWhich cells perform cross-presentation?BackSpecialized dendritic cells
- FrontWhich cells does HIV infect?BackCD4+ T-helper cells plus monocytes/macrophages
- FrontWhat is HIV's primary receptor?BackCD4
- FrontWhat are HIV's co-receptors?BackCXCR4 and CCR5
- FrontWhy are monocytes/macrophages HIV targets and reservoirs?BackThey express CD4
- FrontSerum sickness is which type of hypersensitivity?BackType III (immune-complex-mediated)
- FrontWhat is the underlying mechanism of Type III hypersensitivity?BackCirculating antigen-antibody complexes deposit in tissues
- FrontIn Type III hypersensitivity, which cells arrive first?BackNeutrophils
- FrontWhat mediates the tissue damage in Type III hypersensitivity?BackComplement
- FrontBesides serum sickness, name another Type III reaction.BackThe Arthus reaction
- FrontDelayed-type hypersensitivity (DTH) is which type?BackType IV
- FrontWhich cells mediate Type IV (DTH) hypersensitivity?BackTh1 cells and macrophages
- FrontIs antibody involved in Type IV (DTH) hypersensitivity?BackNo — it is cell-mediated
- FrontAt what time does a DTH reaction peak?Back48-72 hours
- FrontWhat is the correct order of steps in a Western blot?BackElectrophoresis (SDS-PAGE) -> transfer (blotting) -> immunodetection
- FrontIn a competitive ELISA, how does absorbance relate to antigen concentration?BackInversely (absorbance is proportional to 1/antigen)
- FrontWhy is the competitive ELISA relationship inverse?BackMore sample antigen competes off the labeled reagent, lowering signal
- FrontIn a sandwich or indirect ELISA, how does absorbance relate to antigen concentration?BackDirectly (more antigen = higher signal)
- FrontWhich molecule does a naive T cell fail to express that an effector T cell expresses?BackIL-2 receptor (CD25)
- FrontWhen does a T cell acquire the high-affinity IL-2 receptor (CD25)?BackUpon activation
- FrontWhich complement pathways are strictly innate (antibody-independent)?BackAlternative and lectin pathways
- FrontWhich complement pathway requires antibody?BackThe classical pathway
- FrontWhich IgG subclass cannot fix complement?BackIgG4
- FrontOxygen-dependent killing by phagocytes is mediated by which agents?BackReactive oxygen intermediates (ROIs), nitric oxide (NO), and hypochlorous acid (HOCl)
- FrontWhat does the NBT (or DHR) test screen for?BackDefective intracellular oxidative (respiratory-burst) killing by phagocytes
- FrontWhich disease does an abnormal NBT/DHR test diagnose?BackChronic Granulomatous Disease (CGD)
- FrontWhat is the best method to define a cell's phenotype (size, granularity, CD markers)?BackFlow cytometry (FACS)
- FrontIn flow cytometry, what does forward scatter (FSC) measure?BackCell size
- FrontIn flow cytometry, what does side scatter (SSC) measure?BackCell granularity
- FrontWhat separation technique does MACS use?BackMagnetic-bead separation
- FrontIn MACS, what does negative selection isolate?BackThe untouched target cells (unwanted cells are labeled and removed)
- FrontWhat is Ficoll used for?BackDensity-gradient isolation of PBMCs (peripheral blood mononuclear cells)
- FrontIn a sandwich or indirect ELISA, how does absorbance relate to antigen concentration?BackDirectly proportional (absorbance increases with antigen)
- FrontIn a competitive ELISA, how does absorbance relate to antigen concentration?BackInversely proportional (absorbance decreases as antigen increases)
- FrontWhat is the best test for measuring anti-bacterial serum antibody level?BackELISA
- FrontWhat is the correct order of steps in a Western blot?BackElectrophoresis -> transfer -> immunodetection
- FrontWhat does the indirect Coombs test detect?BackMaternal anti-Rh antibody in the serum (pregnancy screen)
- FrontWhat does the direct Coombs test detect?BackAntibody already bound on the RBC surface
- FrontWhich vaccine types can be safely given to immunodeficient patients?BackKilled/inactivated and subunit vaccines
- FrontCan live-attenuated vaccines be given to immunodeficient patients?BackNo - they are contraindicated
- FrontIn which patient groups is live-attenuated vaccine contraindicated?BackImmunodeficiency, pregnancy, and HIV
- FrontWhich vaccine type gives the best cell-mediated (cellular) immune response?BackLive-attenuated vaccines
- FrontWhich infectious disease has been eradicated by vaccination?BackSmallpox
- FrontWhich arm(s) of immunity do mRNA COVID-19 vaccines stimulate?BackBoth humoral and cellular
- FrontWhat does an adjuvant do in a vaccine?BackAugments and prolongs the antigen's effect / recruits APCs, boosting the immune response
- FrontGive an example of a still-used vaccine adjuvant.BackAlum
- FrontWhich vaccines are the oral polio vaccines?BackSabin (oral) and Koprowski
- FrontIs BCG an attenuated vaccine?BackYes, BCG is attenuated
- FrontWhich vaccines are NOT attenuated (whole-cell pertussis, rabies, HepB candidates)?BackPertussis (whole-cell), rabies, and HepB
- FrontWhich immunoglobulin class do B1 lymphocytes produce?BackIgM (natural antibodies)
- FrontWhich immunoglobulin class crosses the placenta?BackIgG only
- FrontWhich isotype dominates the early primary immune response?BackIgM
- FrontAre gingivitis and periodontitis the same condition?BackNo - gingivitis precedes and differs from periodontitis
- FrontWhat is the keystone pathogen of periodontitis?BackPorphyromonas gingivalis
- FrontWhat characterizes severe periodontitis?BackAlveolar bone loss
- FrontWhat antibody causes hemolytic disease of the newborn (HDN)?BackIncomplete (IgG) anti-D antibody
- FrontIn HDN, what is the Rh status of the affected mother?BackRh-negative and sensitized
- FrontIn HDN, what is the Rh status of the affected fetal RBCs that are destroyed?BackRh-positive
- FrontWhy can the anti-D antibody in HDN reach the fetus?BackIt is IgG, which crosses the placenta
- FrontWhich immunoglobulin carries the secretory component?BackSecretory IgA
- FrontFor a 2026 sitting, which IgA subclass is the examiner-preferred key for the secretory component?BackIgA2
- FrontWhich statement about innate immunity recognition is correct?BackIt recognizes both PAMPs and DAMPs
- FrontDoes innate immunity have antigen-specific memory?BackNo (it recognizes conserved patterns, not specific antigens)
- FrontWhat does PAMP stand for?BackPathogen-associated molecular pattern
- FrontGive examples of PAMPs.BackLPS, peptidoglycan, flagellin, dsRNA
- FrontAre PAMPs unique to a single pathogen or shared across microbes?BackShared across many different microbes (conserved structures)
- FrontWhat does DAMP stand for?BackDamage/danger-associated molecular pattern
- FrontWhere do DAMPs come from?BackEndogenous molecules released by stressed/dying host cells
- FrontHow does the diversity of PRRs compare to the TCR?BackPRRs recognize a limited germline-encoded set; the TCR has far greater clonal diversity
- FrontAre PRRs germline-encoded or clonally rearranged?BackGermline-encoded
- FrontWhat is the keyed exam fact about TLR4 and LPS?BackLPS ligation of TLR4 activates APCs
- FrontWhich TLR senses LPS?BackTLR4
- FrontOn which type of bacteria is LPS found?BackGram-negative bacteria
- FrontState the TLR4 signaling chain (LPS to APC).BackLPS → TLR4 → APC activation
- FrontWhich inflammasome activates IL-1β?BackThe NLRP3 inflammasome
- FrontWhat does the NLRP3 inflammasome do to pro-IL-1β?BackProcesses it into active IL-1β
- FrontWhich two cytokines drive the hepatic acute-phase protein response?BackIL-1 and IL-6
- FrontWhich cytokine pairs are distractors for the acute-phase response?BackIL-12+IFN-γ, IL-4+IL-5, TGF-β+IL-10
- FrontIn the single-answer phrasing, which ONE cytokine is keyed for acute-phase protein release?BackIL-6
- FrontWhat causes the vasodilation seen in acute inflammation?BackMast-cell degranulation (releasing histamine/vasoactive mediators)
- FrontWhich leukocyte dominates the site during the first ~6 hours of acute inflammation?BackNeutrophils
- FrontWhich cells arrive later than neutrophils in acute inflammation?BackMacrophages/monocytes
- FrontList the oxygen-dependent (oxidative) killing products of phagocytes.BackReactive oxygen intermediates (ROIs), nitric oxide (NO), hypochlorous acid (HOCl)
- FrontIn the oxidative-killing item, why is myeloperoxidase a distractor?BackIt is the enzyme that makes HOCl, not a reactive species itself
- FrontWhich enzyme generates the superoxide of the respiratory burst in phagocytes?BackNADPH oxidase
- FrontWhat does the NBT (nitro-blue tetrazolium) / DHR test screen for?BackDefective intracellular oxidative (respiratory-burst) killing by phagocytes
- FrontAn abnormal NBT/DHR test points to which disease?BackChronic Granulomatous Disease (CGD)
- FrontWhat is the underlying defect in Chronic Granulomatous Disease?BackDefective NADPH oxidase → failed respiratory burst
- FrontWhy does NBT fail to be reduced in CGD?BackNo reactive oxygen species are generated
- FrontWhich CD marker is found on ALL T cells?BackCD3
- FrontWhat is CD3 part of?BackThe TCR signaling complex
- FrontWhich CD marker defines helper T cells?BackCD4
- FrontOn which non-T cells is CD4 also expressed?BackMonocytes/macrophages
- FrontCD4 is the primary receptor for which virus?BackHIV
- FrontWhat are HIV's co-receptors?BackCXCR4 and CCR5
- FrontWhich CD marker defines cytotoxic T cells?BackCD8
- FrontCytotoxic (CD8) T cells recognize peptide presented on which MHC class?BackMHC class I
- FrontWhich CD marker is the monocyte/macrophage LPS co-receptor?BackCD14
- FrontCD14 works with which TLR in LPS sensing?BackTLR4
- FrontWhich CD marker defines B lymphocytes?BackCD19
- FrontWhich CD marker is the defining phenotypic marker of NK cells?BackCD56
- FrontWhich receptor (not CD56) mediates ADCC on NK cells?BackCD16 (FcγRIII)
- FrontWhich CD marker is found on all T cells?BackCD3
- FrontWhich CD marker defines helper T cells?BackCD4
- FrontBesides helper T cells, which cells also express CD4?BackMonocytes/macrophages
- FrontCD4 is the primary receptor for which virus?BackHIV
- FrontWhich CD marker defines cytotoxic T cells?BackCD8
- FrontWhich CD marker is the monocyte/macrophage LPS co-receptor?BackCD14
- FrontWhich CD marker defines B lymphocytes?BackCD19
- FrontWhich CD marker defines NK cells?BackCD56
- FrontWhich receptor on NK cells mediates ADCC?BackCD16 (FcγRIII)
- FrontName a principal immune function of the macrophage besides phagocytosis.BackAntigen presentation
- FrontWhat is efferocytosis, a macrophage function?BackClearance of apoptotic cells
- FrontWhich professional APC links innate and adaptive immunity via antigen presentation?BackThe macrophage
- FrontMacrophages present antigen on which MHC class?BackMHC class II
- FrontName the tissue macrophage of the liver.BackKupffer cell
- FrontName the tissue macrophage of the CNS/brain.BackMicroglia
- FrontName the bone macrophage-lineage cell that resorbs bone.BackOsteoclast
- FrontWhich cells mediate alveolar bone loss in periodontitis?BackOsteoclasts
- FrontWhich complement pathways are strictly innate (antibody-independent)?BackAlternative and lectin pathways
- FrontWhy is the classical complement pathway not strictly innate?BackIt requires antibody
- FrontWhat triggers the classical complement pathway?BackAntigen-antibody complexes (antibody)
- FrontWith which component does the classical complement pathway begin?BackC1
- FrontAfter C1, which components continue the classical pathway?BackC4 then C2
- FrontC4 and C2 of the classical pathway form which convertase?BackThe C3 convertase
- FrontWhich complement components form the membrane attack complex (MAC)?BackC5b-C9
- FrontWhat does the membrane attack complex (C5b-9) do?BackForms a lytic pore in the target membrane
- FrontThe MAC is the terminal pathway common to how many complement routes?BackAll three
- FrontWhich IgG subclass cannot fix the classical complement pathway?BackIgG4
- FrontBesides IgG4, which immunoglobulin class does not fix the classical pathway?BackIgA
- FrontWhich are the primary (central) lymphoid organs?BackThymus and bone marrow
- FrontWhat defines a primary lymphoid organ?BackWhere lymphocytes develop/mature
- FrontWhere do T cells mature?BackThe thymus
- FrontWhere do B lymphocytes mature?BackThe bone marrow
- FrontWhich adhesion molecules guide lymphocyte homing/extravasation into tissues?BackSelectins (via rolling)
- FrontWhere do dendritic cells primarily present antigen to T cells?BackThe lymph nodes
- FrontLymph nodes are which category of lymphoid organ?BackSecondary lymphoid organs
- FrontWhich cells directly kill virus-infected cells without prior sensitization?BackNK (natural killer) cells
- FrontWhich cytotoxic molecules do NK cells share with CD8 CTLs?BackPerforin and granzyme
- FrontThrough which receptor do NK cells mediate ADCC?BackCD16 (FcγRIII)
- FrontIn ADCC, what does the NK cell CD16 bind?BackThe Fc of IgG coating the target
- FrontWhich cells provide protection against intracellular pathogens?BackT cells and NK cells
- FrontWhat type of inflammatory process drives alveolar bone loss in periodontitis?BackA chronic, cytokine-driven process activating osteoclasts
- FrontWhich mediators drive osteoclast activation in periodontitis?BackIL-1, TNF, IL-6, RANKL
- FrontOn 'periodontitis statements except,' which statement is false?BackThat gingivitis and periodontitis are the same
- FrontWhich condition precedes periodontitis?BackGingivitis
- FrontWhat is the keystone pathogen of periodontitis?BackP. gingivalis
- FrontSevere periodontitis is characterized by what tissue change?BackAlveolar bone loss
- FrontWhat is the best laboratory method to define a cell's phenotype (size, granularity, CD markers)?BackFlow cytometry (FACS)
- FrontIn flow cytometry, what does forward scatter (FSC) measure?BackCell size
- FrontIn flow cytometry, what does side scatter (SSC) measure?BackGranularity
- FrontIn flow cytometry, how is CD-marker expression detected?BackFluorescent antibodies
- FrontWhich region of the antibody molecule binds antigen?BackThe Fab region (fragment antigen-binding)
- FrontWhich antibody region mediates complement fixation, placental transfer, ADCC, and cytophilic binding?BackThe Fc region (fragment crystallizable)
- FrontThe Fc region is the antibody's effector tail made of which structural part?BackThe constant region
- FrontThe constant region of the immunoglobulin heavy chain dictates the antibody's what?BackIts isotype (antibody class)
- FrontWhich antibody property does the heavy-chain constant region determine: isotype, idiotype, or allotype?BackIsotype
- FrontWhich immunoglobulin classes make up the isotypes?BackIgG, IgA, IgM, IgE, IgD
- FrontWhat does an antibody's idiotype refer to?BackIts variable-region/CDR antigen specificity
- FrontWhat does an antibody's allotype refer to?BackAn allelic (genetic) variant
- FrontWhat determines antigen-recognition specificity in the variable region of an antibody?BackThe CDRs (complementarity-determining regions / hypervariable loops)
- FrontWhat part of the antibody do the CDRs form?BackThe antigen-binding paratope
- FrontAnother name for the CDRs (complementarity-determining regions)?BackHypervariable loops
- FrontWhat is the function of immunoglobulins (antibodies) in host defense?BackThey tag antigens for destruction and removal
- FrontAntibodies tag antigens, but which components actually do the killing?BackComplement, phagocytes, and NK cells (ADCC)
- FrontWhich single immunoglobulin class crosses the placenta?BackIgG only
- FrontPlacental transfer of IgG is mediated by which antibody region?BackThe Fc region
- FrontWhat does IgG placental transfer provide to the neonate?BackPassive neonatal immunity
- FrontWhat term describes the Fc-mediated ability of antibody to bind immune-cell surfaces (mast cells, macrophages, NK)?BackCytophilic binding
- FrontIn cytophilic binding, which antibody region adheres to Fc receptors on cells?BackThe Fc region
- FrontIn ADCC against a virus-infected cell, what does the NK cell recognize to trigger killing?BackIgG bound to viral capsid protein on the target cell's plasma membrane
- FrontWhich NK receptor binds the Fc of surface-bound IgG during ADCC?BackCD16 (FcγRIII)
- FrontSecretory IgA protects mucosal surfaces primarily by which mechanism?BackBy preventing microbial adherence to the mucosa
- FrontDoes secretory IgA activate complement?BackNo
- FrontWhat is the molecular form of secretory IgA at mucosal surfaces?BackA dimer joined by a J chain plus a secretory component
- FrontWhen is the secretory component added to IgA?BackDuring epithelial transcytosis
- FrontWhat does the secretory component protect IgA from in secretions?BackProteolysis
- FrontWhich immunoglobulin carries the secretory component and dominates oral-cavity mucosal surveillance?BackSecretory IgA
- FrontIf forced to a subclass, which IgA subclass carries the secretory component (examiner-preferred)?BackIgA2
- FrontWhich immunoglobulin binds strongly to mast cells and mediates Type I hypersensitivity?BackIgE
- FrontIgE binds which high-affinity receptor on mast cells/basophils?BackFcεRI
- FrontDoes IgE fix (activate) complement?BackNo
- FrontIs IgE abundant in saliva?BackNo
- FrontWhat is the defining feature of an antigen-presenting cell (APC)?BackExpression of MHC class II
- FrontProfessional APCs present exogenous peptide on MHC II to which T cells?BackCD4 T cells
- FrontOn which cell types is MHC class II found?BackB cells, dendritic cells (APCs), and macrophages
- FrontWhich cells express MHC class I?BackAll nucleated cells
- FrontMHC class I presents endogenous peptide to which T cells?BackCD8 T cells
- FrontWhat form of antigen does the T-cell receptor (TCR) recognize?BackA linear antigenic peptide in the MHC groove
- FrontWhat form of antigen does the B-cell receptor (BCR) recognize?BackSoluble, native (conformational) antigen directly
- FrontAre T cells MHC-restricted in their antigen recognition?BackYes
- FrontAntigens degraded in the proteasome belong to which processing pathway?BackIntrinsic (endogenous) antigens
- FrontProteasome-degraded (endogenous) peptides are loaded onto which MHC class?BackMHC class I
- FrontTrace the endogenous antigen-processing pathway from degradation to T-cell subset.BackProteasome → endogenous antigen → MHC class I → CD8 T cell
- FrontTrace the exogenous antigen-processing pathway from degradation to T-cell subset.BackEndosome/lysosome → exogenous antigen → MHC class II → CD4 T cell
- FrontWhat does cross-presentation allow?BackActivation of a CD8 T cell by endocytosed (exogenous) antigen
- FrontIn cross-presentation, exogenous antigen is routed onto which MHC class?BackMHC class I
- FrontIn a secondary CD8 cytotoxic response, which cell presents the antigen?BackAn MHC-I-expressing somatic (any nucleated) cell, not a professional APC
- FrontWhich immunoglobulin classes do mature, pre-class-switch (naïve) B cells co-express on their surface?BackIgM and IgD
- FrontWhich immunoglobulin classes do naive (pre-class-switch) B cells co-express on their surface?BackIgM and IgD
- FrontWhich immunoglobulin class is produced by B1 lymphocytes?BackIgM (natural antibodies)
- FrontWhat kind of IgM do B1 cells secrete?BackLow-affinity, polyreactive IgM with little class switching
- FrontWhich immunoglobulin isotype dominates the early primary antibody response?BackIgM
- FrontWhich isotypes does class switching produce in the secondary response?BackIgG, IgA, and IgE
- FrontWhich enzymes mediate V(D)J recombination?BackRAG1 and RAG2 (recombination-activating genes)
- FrontWhat does V(D)J recombination assemble?BackThe variable region, creating pre-antigen receptor diversity
- FrontBy what process does antibody affinity increase during the secondary response?BackSomatic hypermutation of variable-region genes in germinal centers, then selection
- FrontWhere does somatic hypermutation occur?BackIn germinal centers
- FrontDoes affinity maturation use RAG/V(D)J recombination?BackNo
- FrontWhich IgG subclass is unable to fix complement?BackIgG4
- FrontWhich IgG subclasses are the strong classical-pathway complement fixers?BackIgG3 and IgG1 (IgG3 strongest)
- FrontRank IgG1 vs IgG3 for complement-fixing strength.BackIgG3 > IgG1
- FrontWhich IgG subclass is the non-fixer of complement?BackIgG4
- FrontWhat does an antibody titer refer to?BackThe highest dilution of serum that still gives a positive result
- FrontDefine antibody avidity in terms of affinity and valency.BackAvidity = affinity × valency (total binding strength)
- FrontWhat does affinity measure?BackSingle-site binding strength
- FrontWhich immunoglobulin is the classic example of high avidity?BackIgM
- FrontWhich helper cell supports CD8 T-cell activation against a weakly-pathogenic antigen?BackCD4+ Th1 cells
- FrontHow do Th1 cells help prime CD8 against low-danger antigens?BackThey license the APC and provide help (IL-2, CD40L)
- FrontWhat transmits information about an antigen's pathogenicity to T cells?BackCostimulatory molecules expressed by APCs after TLR stimulation
- FrontWhich costimulatory molecules constitute signal 2 to T cells?BackB7 / CD80-86
- FrontWhat upregulates B7/CD80-86 on APCs?BackTLR sensing of PAMPs
- FrontIn an antigen-antibody precipitation reaction, what is the physical state of the antigen?BackSoluble antigen
- FrontWhat does soluble antigen form when it reacts with antibody in precipitation?BackAn insoluble lattice that precipitates out of solution
- FrontIn an agglutination reaction, what is the physical state of the antigen?BackParticulate antigen
- FrontWhat happens to particulate antigen when antibody crosslinks it?BackIt clumps (agglutinates)
- FrontDiscriminate precipitation vs agglutination by antigen type.BackPrecipitation = soluble antigen lattice; agglutination = particulate antigen clumps
- FrontBlood typing (ABO/Rh) is an example of which antigen-antibody reaction?BackAgglutination
- FrontWhy is blood typing agglutination rather than precipitation?BackRBCs are particulate antigens
- FrontThe latex syphilis test is an example of which antigen-antibody reaction?BackAgglutination
- FrontMeasuring a bacterial titer (clumping of whole bacteria) is which reaction type?BackAgglutination
- FrontWhy is a bacterial titer an agglutination reaction?BackWhole bacteria are particulate antigens
- FrontWhat does a high bacterial agglutination titer reflect?BackA secondary (anamnestic) antibody response
- FrontName the three classic lab examples of agglutination reactions.BackBlood typing, latex syphilis test, and bacterial titer
- FrontWhich laboratory technique is used to quantify antigen or antibody?BackRadial immunodiffusion
- FrontIn radial immunodiffusion, what is the ring diameter proportional to?BackAntigen concentration
- FrontWhat is the primary function of radial immunodiffusion?BackTo quantify antigen or antibody concentration
- FrontWhat type of method is radial immunodiffusion?BackA precipitation-in-gel method
- FrontWhat two principles does immunoelectrophoresis combine?BackElectrophoretic separation of antigens followed by immunodiffusion
- FrontIn immunoelectrophoresis, on what basis are antigens electrophoretically separated?BackBy charge and size
- FrontWhat forms where separated antigen meets specific antibody in immunoelectrophoresis?BackPrecipitation arcs
- FrontHow is antibody titer defined?BackThe highest dilution of serum that still gives a positive result
- FrontA high bacterial agglutination titer indicates which type of immune response?BackA secondary (anamnestic) response
- FrontWhy does a high agglutination titer indicate a secondary response?BackHigh antibody levels reflect prior sensitization/memory
- FrontBoth precipitation and agglutination depend on which fundamental antibody property?BackAntibody bivalency/multivalency enabling crosslinking of antigen
- FrontWith soluble antigen, antibody crosslinking produces what?BackA lattice (precipitation)
- FrontWith particulate antigen, antibody crosslinking produces what?BackClumps (agglutination)
- FrontIn a secondary CD8+ cytotoxic response, the antigen is presented on which type of cell?BackAn MHC class I-expressing somatic (any nucleated) cell, not a professional APC
- FrontWhich MHC class restricts the cytotoxic CD8+ T-cell secondary effector response?BackMHC class I
- FrontWhich cells express MHC class I (presenting endogenous peptide to CD8 effectors)?BackAll nucleated (somatic) cells
- FrontWhy is the secondary CD8 killing target a somatic cell rather than a professional APC?BackEffector CTLs recognize endogenous peptide on MHC-I of the infected somatic target and kill it directly
- FrontDoes the secondary CD8 kill require a professional MHC-II APC?BackNo
- FrontADCC against a virus-infected cell is induced by which specifically bound molecule?BackIgG bound to viral capsid protein on the target cell's plasma membrane
- FrontIn ADCC, which receptor on the NK cell engages the Fc of the surface-bound IgG?BackCD16 (FcγRIII)
- FrontIn ADCC of a virus-infected cell, where must the antibody-bound antigen be located?BackOn the target cell's plasma membrane (surface)
- FrontWhy can't intracellular/cytoplasmic antigen trigger ADCC?BackIt is inaccessible to antibody
- FrontWhich antibody isotype mediates ADCC against a virus-infected cell?BackIgG
- FrontThrough which effector receptor does the NK cell engage IgG in ADCC?BackCD16 (FcγRIII)
- FrontName the two distinct cytotoxic killing routes used by CTLs and NK cells.BackPerforin/granzyme (granule-exocytosis) pathway and the FasL-Fas death-receptor pathway
- FrontBesides FasL-Fas, which other receptor pair acts in the death-receptor killing route?BackTNF-TNFR
- FrontBoth CTL/NK killing pathways converge on what fate for the target cell?BackApoptosis
- FrontWhat is the role of perforin in CTL/NK killing?BackIt polymerizes to form pores in the target membrane
- FrontWhat is the role of granzymes in CTL/NK killing?BackSerine proteases that enter via perforin pores and trigger the caspase apoptosis cascade
- FrontThe perforin/granzyme killing route is also called what?BackThe granule-exocytosis (granule-dependent) route
- FrontWhich CTL killing pathway is receptor-dependent rather than granule-dependent?BackThe FasL-Fas (CD95) death-receptor pathway
- FrontIn the FasL-Fas pathway, what does CTL FasL engage on the target?BackFas (CD95)
- FrontWhat does Fas engagement on the target trigger?BackThe death-receptor caspase cascade leading to apoptosis
- FrontDo NK cells and CD8+ CTLs share cytotoxic machinery?BackYes — both use perforin/granzyme and FasL-Fas
- FrontHow does NK recognition differ from CTL recognition?BackNK killing is MHC-I-independent (missing-self); CTL killing is MHC-I-restricted/antigen-specific
- FrontWhich lymphocyte kills virally-infected cells directly without prior sensitization or MHC restriction?BackNK cells
- FrontBy what recognition mechanism do NK cells target cells?BackMissing-self recognition (innate)
- FrontDTH (delayed-type hypersensitivity) is classified as which hypersensitivity type?BackType IV
- FrontDTH is mediated by antibody or by cells?BackCell-mediated (T-cell), not antibody
- FrontWhat is the time course of a delayed-type hypersensitivity reaction?BackDelayed, 24-72 hours
- FrontWhich cells mediate DTH / Type IV hypersensitivity?BackTh1 cells + macrophages
- FrontHow do Th1 cells recruit and activate macrophages in DTH?BackBy releasing IFN-γ
- FrontWhat is the molecular trigger of allergic contact dermatitis?BackA hapten binding a skin self-protein (carrier) to form a complete immunogen
- FrontAllergic contact dermatitis is which hypersensitivity type and T-cell subset?BackType IV (DTH), Th1-mediated
- FrontMetal braces, crowns, and dental fillings may induce which immune reaction?BackDelayed-type hypersensitivity (DTH / Type IV)
- FrontHow do metal ions in dental materials trigger DTH?BackThey act as haptens binding oral/skin self-proteins, driving a Th1 + macrophage contact reaction
- FrontContact dermatitis is which hypersensitivity type?BackType IV (DTH)
- FrontContact dermatitis is mediated by which T helper subset?BackTh1 (with macrophages as effectors)
- FrontWhich cytokines drive naïve CD4+ T-cell differentiation toward Th1?BackIL-12 (from APCs/macrophages) and IFN-γ
- FrontWhich transcription factor commits CD4+ T cells to the Th1 lineage?BackT-bet
- FrontTh1 differentiation supports which type of immunity?BackCell-mediated immunity
- FrontWhich cytokine drives naïve CD4+ T-cell differentiation toward Th2?BackIL-4
- FrontWhich transcription factor commits CD4+ T cells to the Th2 lineage?BackGATA3
- FrontTh2 differentiation supports which type of responses?BackHumoral/allergic responses
- FrontSuppression of Th1 by Th2 is mediated by which cytokine?BackIL-10
- FrontWhat is the cellular source of the IL-10 that suppresses Th1?BackTh2 cells
- FrontWhich Th1 cytokine cross-regulates (suppresses) Th2?BackIFN-gamma
- FrontWhich Th2-derived cytokine suppresses Th1?BackIL-10
- FrontWhat is the result of the mutual Th1/Th2 cross-regulation called?BackImmune deviation
- FrontIs CD8+ cytotoxic killing of virally-infected cells a Th1 or Th2 function?BackTh1 (cell-mediated)
- FrontWhich arm of immunity does a Th2 response drive?BackHumoral / IgE / eosinophil responses
- FrontWhich CD4+ T-cell subset recruits and activates macrophages (phagocytes)?BackTh1
- FrontWhich cytokines does Th1 secrete to recruit/activate macrophages?BackIFN-gamma and IL-2
- FrontWhat is the principal macrophage-activating signal from Th1 cells?BackIFN-gamma
- FrontWhat does IFN-gamma do to macrophages?BackActivates them, enhancing microbicidal/oxidative killing
- FrontWhat is the primary autocrine T-cell growth/proliferation cytokine from activated Th1 cells?BackIL-2
- FrontWhat does IL-2 do for T cells?BackDrives clonal proliferation of activated T cells
- FrontWhich receptor marks activated/effector T cells (not naive T cells)?BackIL-2R (CD25)
- FrontActivation of a CD8+ T cell against a weakly-pathogenic antigen is supported by which helper cell?BackCD4+ Th1
- FrontWhy does CD8 activation by a weak antigen require Th1 help?BackWeak antigens cannot fully license the APC alone
- FrontWhat does CD4+ Th1 provide to enable CD8 priming against weak antigens?BackIL-2 and CD40L-mediated APC licensing/costimulation
- FrontWhich Th subset orchestrates immunity to intracellular pathogens?BackTh1
- FrontWhat cytokines drive Th1 differentiation?BackIL-12 and IFN-gamma
- FrontHow does Th1 fight intracellular microbes?BackActivates macrophages and supports CD8 CTLs
- FrontWhich Th subset handles extracellular/parasitic/allergic responses?BackTh2
- FrontHow does NK cell killing recognize targets (relative to MHC-I)?BackMHC-I-independent 'missing-self' (kills cells that down-regulate MHC-I)
- FrontHow does CD8 CTL killing recognize targets (relative to MHC-I)?BackMHC-I-restricted, antigen-specific (kills cells presenting peptide on MHC-I)
- FrontWhat effector machinery do NK cells and CD8 CTLs share?BackPerforin/granzyme and Fas
- FrontSerum sickness and Arthus reactions are which hypersensitivity type?BackType III (immune-complex)
- FrontDelayed-type hypersensitivity (DTH) is which hypersensitivity type?BackType IV (cell-mediated)
- FrontWhich cells mediate Type IV DTH?BackTh1 + macrophages
- FrontWhat are the four mechanisms of autotolerance (self-tolerance)?BackClonal deletion, clonal anergy, active suppression (Tregs), sequestration of antigens
- FrontIs 'immune paralysis' one of the four keyed autotolerance mechanisms?BackNo
- FrontIs 'exhaustion of memory cells/clones' one of the four keyed autotolerance mechanisms?BackNo
- FrontIs 'positive/negative selection' the keyed answer for the four mechanisms of autotolerance?BackNo
- FrontWhat does immunological paralysis refer to?BackSubliminal-threshold unresponsiveness
- FrontWhich tolerance mechanism is broken in atopic (allergic) individuals?BackImmunological facilitation
- FrontHow do Tregs enforce/support clonal anergy (molecular mechanism)?BackTheir CTLA-4 (CD152) binds CD80/CD86 (B7) on the APC
- FrontBy binding B7, what does Treg CTLA-4 outcompete?BackCD28 costimulation
- FrontWhat is the CD designation for CTLA-4?BackCD152
- FrontWhich APC ligands does Treg CTLA-4 (CD152) bind to enforce anergy?BackCD80 and CD86 (the B7 molecules)
- FrontWhat is the CD designation for CTLA-4?BackCD152
- FrontOn the APC, which molecules does CTLA-4 (CD152) bind?BackCD80/86 (B7)
- FrontWhat does Treg CTLA-4 (CD152) enforce by binding the APC?BackClonal anergy
- FrontWhich ligands on the APC does Treg CTLA-4 bind to enforce anergy?BackCD80 and CD86 (the B7 molecules)
- FrontWhat is the alternative name for the B7 molecules?BackCD80 and CD86
- FrontTregs support clonal anergy by binding what on the APC?BackCD80/86 (B7)
- FrontTregs bind CD80/86 on the APC using which of their molecules?BackCD152 (CTLA-4)
- FrontWhat two-signal event defines clonal anergy at the T-cell level?BackSignal 1 (TCR-peptide/MHC) without signal 2 (costimulation)
- FrontWhat provides signal 2 (costimulation) for T-cell activation?BackCD28 binding CD80/86
- FrontA naive T cell gets signal 1 but no costimulation - what is the outcome?BackClonal anergy (functional unresponsiveness)
- FrontWhere does central tolerance occur?BackPrimary lymphoid organs (thymus for T cells, bone marrow for B cells)
- FrontHow is central tolerance generated for T cells?BackNegative selection in the thymus
- FrontIn thymic negative selection, which T-cell clones are deleted?BackThose binding self-peptide on self-MHC too strongly
- FrontThymic negative selection is an example of which tolerance mechanism?BackClonal deletion
- FrontWhere are self-reactive B cells deleted during central tolerance?BackBone marrow
- FrontWhere is peripheral tolerance maintained?BackOutside the primary lymphoid organs
- FrontWhich clones does peripheral tolerance act on?BackSelf-reactive clones that escaped central deletion
- FrontName the three mechanisms of peripheral tolerance.BackClonal anergy, Treg active suppression, antigen sequestration
- FrontWhich tolerance mechanisms are central (thymus/bone marrow)?BackClonal deletion (negative selection)
- FrontWhich tolerance mechanisms are peripheral?BackClonal anergy, Treg active suppression, antigen sequestration
- FrontWhat is the classic example of an immunologically privileged site?BackThe testis
- FrontWhat is an immunologically privileged site?BackAn anatomical site sequestered from immune surveillance
- FrontWhich tolerance mechanism do privileged sites represent?BackAntigen sequestration
- FrontDefine immune ignorance as a tolerance state.BackSelf-reactive lymphocytes coexist with self-antigen but do not respond
- FrontWhy does a clone ignore its self-antigen in immune ignorance?BackAntigen is below the concentration/location threshold to trigger activation
- FrontDefine immunological paralysis.BackUnresponsiveness produced by antigen at a subliminal threshold (e.g., very high/persistent dose)
- FrontIs immunological paralysis the same as anergy?BackNo - it is a distinct term
- FrontIs immunological paralysis part of the four-part autotolerance list?BackNo
- FrontIs immunological paralysis a recognized peripheral-tolerance term?BackYes (subliminal-threshold unresponsiveness)
- FrontDefine the anamnestic response.BackThe faster, stronger immune response on re-exposure to a previously encountered antigen
- FrontWhich cells mediate the anamnestic response?BackMemory lymphocytes
- FrontName the two principal mechanisms by which autoimmunity arises.BackMolecular mimicry and release of sequestered antigens
- FrontWhat is molecular mimicry as an autoimmunity mechanism?BackA microbial antigen resembles a self-antigen, so the anti-microbial response cross-reacts with self
- FrontHow does release of sequestered antigen cause autoimmunity?BackTrauma/infection exposes hidden self-antigens the immune system never became tolerant to
- FrontGive examples of privileged sites whose antigen release can trigger autoimmunity.BackTestis, eye, brain
- FrontWhich immunoglobulin is associated with self-reactivity (natural autoantibodies)?BackSelf-reactive IgM
- FrontActive suppression as an autotolerance mechanism is carried out by which cells?BackTregs (regulatory T cells)
- FrontWhere are self-reactive T cells deleted by clonal deletion?BackThe thymus (negative selection)
- FrontWhere are self-reactive B cells deleted by clonal deletion?BackThe bone marrow
- FrontWhat is clonal deletion?BackPhysical removal of self-reactive clones (central tolerance)
- FrontIn clonal deletion, what happens to the self-reactive clone?BackIt is physically removed/killed
- FrontIn clonal anergy, what happens to the self-reactive clone?BackIt survives but is rendered functionally unresponsive
- FrontClonal anergy results from which signaling pattern?BackSignal 1 without signal 2
- FrontWhat reinforces clonal anergy beyond signal 1 without signal 2?BackTreg CTLA-4
- FrontHow many classes of hypersensitivity reactions are there?BackFour (Types I-IV)
- FrontType I hypersensitivity: principal antibody?BackIgE
- FrontType I hypersensitivity: principal effector cell?BackMast cells (and basophils)
- FrontType I hypersensitivity is also called what?BackImmediate (anaphylactic/atopic) hypersensitivity
- FrontWhat is the timing of Type I hypersensitivity?BackWithin minutes of re-exposure
- FrontWhat triggers the Type I reaction at the cellular level?BackIgE-triggered mast-cell degranulation
- FrontGive two classic clinical examples of Type I hypersensitivity.BackAtopic dermatitis and anaphylaxis
- FrontAtopic dermatitis is which hypersensitivity type?BackType I (IgE/mast-cell mediated)
- FrontContact dermatitis vs atopic dermatitis: which is Type IV?BackContact dermatitis (atopic dermatitis is Type I)
- FrontWhat triggers mast-cell mediator release in Type I hypersensitivity?BackAllergen cross-linking IgE bound to mast-cell FcεRI receptors
- FrontWhat mediators are released on mast-cell degranulation in Type I?BackHistamine and other mediators
- FrontIgE antibody: what is its defining property?BackBinds strongly to mast cells
- FrontDoes IgE fix complement?BackNo
- FrontIs IgE abundant in saliva?BackNo
- FrontIgE mediates which hypersensitivity type (Type I or IV)?BackType I
- FrontBesides allergy, what immune defense is the IgE/mast-cell axis tied to?BackAnti-helminth (parasite) defense
- FrontWhich cell type joins IgE and mast cells in anti-parasite defense?BackEosinophils
- FrontWhich tolerance mechanism is broken in atopic (allergic) individuals?BackImmunological facilitation
- FrontType II hypersensitivity: what is the target of the antibody?BackAn antigen ON a cell or tissue (cell-surface/matrix antigen)
- FrontType II vs Type III: which involves antibody against a cell-bound antigen?BackType II (Type III is against soluble antigen)
- FrontType II hypersensitivity: what are the main effector mechanisms of damage?BackComplement activation, phagocytes (opsonization), and ADCC
- FrontName two classic clinical examples of Type II hypersensitivity.BackHemolytic disease of the newborn (HDN) and transfusion reactions
- FrontTransfusion reactions are which hypersensitivity type?BackType II
- FrontWhy are transfusion reactions Type II?BackAnti-A/anti-B antibody binds antigens on transfused RBC surface
- FrontWhat destroys the RBCs in a transfusion reaction?BackComplement-mediated lysis and phagocytic clearance
- FrontType III hypersensitivity: what is the causative immune structure?BackImmune complexes (antibody bound to soluble antigen)
- FrontIn Type III hypersensitivity, what kind of antigen does antibody bind?BackSoluble antigen
- FrontIn Type III hypersensitivity, which cells arrive first at the site?BackNeutrophils (PMNs)
- FrontIn Type III, how is tissue damage actually produced?BackDeposited immune complexes activate complement, attracting neutrophils whose enzymes damage tissue
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