Which cell is the main antigen-presenting cell capable of activating naive T cells?
A. Neutrophil
B. Dendritic cell
C. Plasma cell
D. Eosinophil
Answer: B. Dendritic cell
Explanation: Dendritic cells express high levels of MHC I/II and costimulatory molecules (CD80/86) and migrate to lymph nodes to activate naive CD4+ and CD8+ T cells.
Class switching of immunoglobulins in B cells requires interaction between CD40 on B cells and which ligand?
A. CD28
B. CD40L (CD154) on T cells
C. CTLA-4
D. FasL
Answer: B. CD40L (CD154) on T cells
Explanation: CD40–CD40L interaction plus cytokines (e.g., IL-4, IFN-γ) drives isotype switching and affinity maturation in germinal centers.
Which immunoglobulin is most abundant in secretions (mucosal immunity)?
A. IgG
B. IgA (dimeric)
C. IgM
D. IgE
Answer: B. IgA (dimeric)
Explanation: Secretory IgA (dimer with J chain) is transported across mucosal epithelium and neutralizes pathogens at mucosal surfaces.
Which complement pathway is initiated by antigen–antibody complexes?
A. Alternative pathway
B. Lectin pathway
C. Classical pathway
D. Terminal pathway
Answer: C. Classical pathway
Explanation: The classical pathway is triggered by IgM or IgG bound to antigen, engaging C1 complex; lectin is by mannose-binding lectin; alternative is spontaneous C3 hydrolysis.
A patient with recurrent Neisseria infections likely has a deficiency of which complement component?
A. C3
B. C5–C9 (MAC)
C. Factor B
D. C1 inhibitor
Answer: B. C5–C9 (MAC)
Explanation: Membrane attack complex (C5b–C9) deficiency predisposes to recurrent Neisseria (Neisseria meningitidis) due to impaired MAC-mediated lysis.
Which cytokine is the main driver of Th1 differentiation?
A. IL-4
B. IL-12
C. TGF-β
D. IL-10
Answer: B. IL-12
Explanation: IL-12 from macrophages/dendritic cells stimulates naive CD4+ T cells to differentiate into Th1 cells (IFN-γ producers), enhancing cell-mediated immunity.
Which immunoglobulin appears first during a primary immune response?
A. IgA
B. IgG
C. IgM
D. IgE
Answer: C. IgM
Explanation: IgM is produced early as pentameric form before class switching to IgG, IgA, or IgE.
Which molecule is necessary for MHC I antigen presentation to CD8+ T cells?
A. TAP (transporter associated with antigen processing)
B. Invariant chain
C. HLA-DM
D. Cathepsin
Answer: A. TAP
Explanation: TAP transports cytosolic peptides into the ER for loading onto MHC I; defects (e.g., Bare Lymphocyte Syndrome I) reduce MHC I surface expression.
Which hypersensitivity type is mediated by IgE and mast cell degranulation?
A. Type I
B. Type II
C. Type III
D. Type IV
Answer: A. Type I
Explanation: Type I (immediate) hypersensitivity: antigen cross-links IgE bound to FcεRI on mast cells → histamine, leukotrienes → anaphylaxis, allergic asthma.
Which cell type is primarily responsible for granuloma formation (epithelioid granulomas)?
A. Neutrophil
B. Eosinophil
C. Macrophage (activated) / epithelioid cells
D. NK cell
Answer: C. Macrophage (activated) / epithelioid cells
Explanation: Persistent Th1 response and IFN-γ activate macrophages to form epithelioid cells and multinucleated giant cells in granulomas.
Which receptor on T cells provides a major inhibitory signal after binding B7 on APCs?
A. CD28
B. CTLA-4 (CD152)
C. CD40L
D. LFA-1
Answer: B. CTLA-4 (CD152)
Explanation: CTLA-4 binds B7 (CD80/86) with greater affinity than CD28, delivering inhibitory signal to downregulate T-cell activation.
Which immunodeficiency is characterized by absence of B cells and low immunoglobulins due to BTK mutation?
A. X-linked agammaglobulinemia (Bruton's)
B. Common variable immunodeficiency
C. Hyper-IgM syndrome
D. Selective IgA deficiency
Answer: A. X-linked agammaglobulinemia (Bruton's)
Explanation: BTK mutation prevents B-cell maturation → very low/absent B cells and immunoglobulins; presents after maternal IgG wanes.
Which vaccine uses attenuated live organisms?
A. Tetanus toxoid
B. Inactivated polio (IPV)
C. MMR (measles-mumps-rubella)
D. Hepatitis B recombinant
Answer: C. MMR (measles-mumps-rubella)
Explanation: MMR is a live attenuated vaccine inducing strong cellular and humoral immunity; contraindicated in severe immunosuppression and pregnancy.
Which immunoglobulin is primarily responsible for opsonization and complement activation?
A. IgA
B. IgD
C. IgG
D. IgM
Answer: C. IgG
Explanation: IgG opsonizes pathogens (Fcγ receptor binding) and activates classical complement pathway; IgM is also efficient at complement activation.
An 18-month-old boy has high IgM, low IgG/IgA, and recurrent sinopulmonary infections; which defect is most likely?
A. CD40L deficiency (Hyper-IgM syndrome)
B. Bruton's agammaglobulinemia
C. Selective IgA deficiency
D. SCID
Answer: A. CD40L deficiency (Hyper-IgM syndrome)
Explanation: Lack of CD40L on T cells prevents class switching, causing elevated or normal IgM with low IgG/IgA and susceptibility to opportunistic infections.
Which cell-surface marker identifies helper T cells?
A. CD8
B. CD3
C. CD4
D. CD16
Answer: C. CD4
Explanation: CD4+ T cells are helper T cells that recognize antigens presented on MHC II; CD8 marks cytotoxic T cells.
Which of the following is a pattern recognition receptor that senses bacterial lipopolysaccharide (LPS)?
A. RIG-I
B. TLR4
C. NOD2
D. TLR9
Answer: B. TLR4
Explanation: TLR4 recognizes LPS (Gram-negative bacteria) with MD-2 and CD14 coreceptor, triggering innate immune responses via NF-κB.
Which HLA allele is strongly associated with ankylosing spondylitis?
A. HLA-B27
B. HLA-DR4
C. HLA-DR3
D. HLA-A3
Answer: A. HLA-B27
Explanation: HLA-B27 is linked to seronegative spondyloarthropathies (ankylosing spondylitis, reactive arthritis).
Which cell type kills virally infected cells without prior sensitization and recognizes low MHC I?
A. CD8+ T cell
B. NK cell
C. B cell
D. Macrophage
Answer: B. NK cell
Explanation: NK cells mediate innate cytotoxicity, detect decreased MHC I and activate through activating receptors to release perforin/granzyme.
Which cytokine produced by Th2 cells promotes B-cell class switching to IgE?
A. IFN-γ
B. IL-4
C. IL-2
D. TNF-α
Answer: B. IL-4
Explanation: IL-4 (and IL-13) drive Th2 responses and class switching to IgE (and IgG4 in humans), promoting allergic responses and helminth defense.
Which of these is a cell-surface marker of B cells?
A. CD3
B. CD19
C. CD8
D. CD16
Answer: B. CD19
Explanation: CD19 is a pan–B-cell marker used clinically to identify B cells; CD3 marks T cells.
Which molecule prevents complement activation on host cells by accelerating decay of C3 convertases?
A. Properdin
B. Factor H
C. Factor B
D. C1 inhibitor
Answer: B. Factor H
Explanation: Factor H (and factor I) regulate alternative pathway by inactivating C3b; properdin stabilizes convertase.
What is the effector mechanism in type II hypersensitivity?
A. Immune-complex deposition
B. IgE–mediated mast cell degranulation
C. Antibody-mediated cell destruction or dysfunction
D. T-cell mediated delayed hypersensitivity
Answer: C. Antibody-mediated cell destruction or dysfunction
Explanation: Type II: IgG or IgM against cell-surface or matrix antigens → complement activation, opsonization, ADCC, or functional blockade/activation (e.g., Graves’ disease).
Which immunodeficiency features severe recurrent viral/fungal infections, chronic diarrhea, failure to thrive, and very low lymphocyte counts including absent thymic shadow?
A. X-linked agammaglobulinemia
B. Common variable immunodeficiency
C. Severe combined immunodeficiency (SCID)
D. DiGeorge syndrome
Answer: C. Severe combined immunodeficiency (SCID)
Explanation: SCID has defective T- and B-cell function (various causes like ADA deficiency, IL-2Rγ mutation) leading to severe opportunistic infections.
Which vaccine type is safest for immunocompromised patients?
A. Live attenuated vaccines
B. Inactivated/killed vaccines
C. Replicating viral vector vaccines
D. Live bacterial vaccines
Answer: B. Inactivated/killed vaccines
Explanation: Inactivated vaccines cannot replicate and are generally safe in immunocompromised hosts, though immune response may be blunted.
Which cell produces large amounts of IFN-γ to activate macrophages in intracellular infections?
A. Th1 CD4+ T cells
B. Th2 CD4+ T cells
C. B cells
D. Eosinophils
Answer: A. Th1 CD4+ T cells
Explanation: Th1 cells (driven by IL-12) secrete IFN-γ to activate macrophages and promote cell-mediated immunity against intracellular pathogens.
Which antibody is primarily responsible for complement activation through the classical pathway?
A. IgA
B. IgE
C. IgG and IgM (especially IgM)
D. IgD
Answer: C. IgG and IgM (especially IgM)
Explanation: IgM (pentameric) is particularly efficient at activating complement; IgG subclasses can also activate classical pathway.
Which leukocyte adhesion molecule deficiency causes recurrent bacterial infections and delayed separation of the umbilical cord?
A. Selectin deficiency
B. LFA-1 (CD18) deficiency — Leukocyte Adhesion Deficiency type 1 (LAD-1)
C. Integrin overexpression
D. ICAM deficiency
Answer: B. LFA-1 (CD18) deficiency — LAD-1
Explanation: LAD-1 due to CD18 mutation prevents neutrophil extravasation, causing absent pus, recurrent infections, and delayed umbilical separation.
Which molecule presents peptides derived from extracellular proteins?
A. MHC I
B. MHC II
C. TAP transporter
D. Proteasome
Answer: B. MHC II
Explanation: MHC II (on APCs) presents peptides from endocytosed extracellular proteins to CD4+ T cells; MHC I presents endogenous peptides to CD8+ T cells.
Which cytokine is central to promoting regulatory T-cell (Treg) differentiation and immune tolerance?
A. IL-17
B. IL-2 and TGF-β
C. IL-4
D. IL-12
Answer: B. IL-2 and TGF-β
Explanation: TGF-β with low IL-6 favors Treg differentiation (FoxP3+), promoting peripheral tolerance; IL-2 supports Treg survival.
Which receptor on B cells binds the Fc portion of IgG to mediate feedback inhibition of antibody production?
A. FcγRIIB (CD32B)
B. FcεRI
C. FcαR
D. FcRn
Answer: A. FcγRIIB (CD32B)
Explanation: FcγRIIB is an inhibitory Fc receptor on B cells; crosslinking to surface Ig reduces B-cell activation and antibody production.
What is the hallmark feature of systemic lupus erythematosus (SLE) immunopathology?
A. T-cell mediated granulomas
B. Immune complex deposition (type III hypersensitivity)
C. IgE-mediated allergy
D. Complement deficiency only
Answer: B. Immune complex deposition (type III hypersensitivity)
Explanation: SLE features immune-complex deposition in kidneys, skin, vessels triggering complement activation and inflammation.
Which is a primary lymphoid organ where T cells mature?
A. Spleen
B. Thymus
C. Lymph node
D. Peyer patches
Answer: B. Thymus
Explanation: T-cell progenitors migrate to thymus for positive and negative selection to establish central tolerance and TCR repertoire.
Which immunoglobulin crosses the placenta and provides passive immunity to the fetus?
A. IgM
B. IgA
C. IgG
D. IgE
Answer: C. IgG
Explanation: Maternal IgG is transported across placenta via FcRn receptor, conferring neonatal protection.
Which laboratory test result best supports diagnosis of complement-mediated autoimmune hemolytic anemia?
A. Negative direct antiglobulin (Coombs) test
B. Positive direct Coombs test for IgG and/or complement on RBCs
C. Elevated IgA only
D. Low reticulocyte count
Answer: B. Positive direct Coombs test for IgG and/or complement on RBCs
Explanation: Direct antiglobulin test detects antibodies or complement on RBC surfaces, confirming immune hemolysis.
Which cytokine is chiefly responsible for fever and acute-phase reactant production?
A. IL-10
B. IL-6
C. IFN-α
D. TGF-β
Answer: B. IL-6
Explanation: IL-6 stimulates hepatocytes to produce CRP, fibrinogen; it also contributes to fever via hypothalamic action.
Which is the primary function of toll-like receptors (TLRs)?
A. Antigen presentation on MHC II
B. Recognition of pathogen-associated molecular patterns (PAMPs) to activate innate immunity
C. Activation of B-cell isotype switching
D. Killing infected cells directly
Answer: B. Recognition of pathogen-associated molecular patterns (PAMPs) to activate innate immunity
Explanation: TLRs detect PAMPs (LPS, dsRNA, unmethylated CpG DNA) and trigger inflammatory signaling (NF-κB, interferon responses).
Which immunodeficiency is caused by a defect in adenosine deaminase (ADA)?
A. X-linked agammaglobulinemia
B. SCID (ADA deficiency)
C. Hyper-IgM syndrome
D. Chronic granulomatous disease
Answer: B. SCID (ADA deficiency)
Explanation: ADA deficiency causes toxic accumulation of adenosine metabolites → lymphocyte apoptosis → SCID with severe combined immunodeficiency.
Which cell-surface molecule interacts with B7 (CD80/86) to provide costimulation for T-cell activation?
A. CD28
B. CTLA-4
C. PD-1
D. CD3
Answer: A. CD28
Explanation: CD28 on T cells binds B7 on APCs for costimulatory signal; without signal 2, T cells become anergic.
Which autoantibody is most specific for pernicious anemia?
A. Anti-mitochondrial antibody
B. Anti-intrinsic factor antibody
C. Anti-dsDNA antibody
D. Anti-smooth muscle antibody
Answer: B. Anti-intrinsic factor antibody
Explanation: Autoantibodies to intrinsic factor (or gastric parietal cells) impair B12 absorption leading to megaloblastic anemia.
Which cell type is the primary producer of IL-17 in mucosal immunity?
A. Th1 cells
B. Th2 cells
C. Th17 cells
D. Treg cells
Answer: C. Th17 cells
Explanation: Th17 cells (driven by IL-6 + TGF-β) produce IL-17 which recruits neutrophils and is important in defense against extracellular bacteria and fungi.
Which laboratory abnormality is characteristic of chronic granulomatous disease (CGD)?
A. Low immunoglobulins
B. Absent oxidative burst on nitroblue tetrazolium (NBT) or dihydrorhodamine (DHR) test
C. Reduced complement levels
D. Low T-cell count
Answer: B. Absent oxidative burst on nitroblue tetrazolium (NBT) or dihydrorhodamine (DHR) test
Explanation: CGD involves NADPH oxidase defects → impaired respiratory burst → recurrent catalase-positive infections and granuloma formation.
Which chemokine receptor is used by HIV to enter macrophages?
A. CXCR4
B. CCR5
C. CXCL8
D. CCR7
Answer: B. CCR5
Explanation: R5-tropic HIV strains use CCR5 (macrophage-tropic) usually early in infection; CXCR4 is used by T-tropic strains later.
What is the mechanism of action of rituximab?
A. Anti–TNF-α antibody
B. Anti-CD20 monoclonal antibody causing B-cell depletion
C. CTLA-4 agonist
D. IL-6 receptor blocker
Answer: B. Anti-CD20 monoclonal antibody causing B-cell depletion
Explanation: Rituximab targets CD20 on B cells causing depletion via ADCC, complement activation, and apoptosis; used in B-cell lymphomas, autoimmune diseases.
Which immunoglobulin is associated with type I hypersensitivity and parasite defense?
A. IgG
B. IgA
C. IgE
D. IgM
Answer: C. IgE
Explanation: IgE binds FcεRI on mast cells and basophils; crosslinking causes degranulation—important in allergic reactions and helminth defense via eosinophils.
Which of the following best describes central tolerance?
A. Deletion or editing of self-reactive lymphocytes during development in primary lymphoid organs
B. Suppression of immune responses by Tregs in peripheral tissues
C. Immune complex clearance in spleen
D. Antibody feedback inhibition
Answer: A. Deletion or editing of self-reactive lymphocytes during development in primary lymphoid organs
Explanation: Central tolerance occurs in thymus (T cells) and bone marrow (B cells) via negative selection to eliminate high-affinity self-reactive clones.
Which of the following is a function of interferon-alpha (IFN-α)?
A. Induces class switching to IgE
B. Promotes antiviral state in cells and activates NK cells
C. Stimulates macrophage oxidative burst only
D. Acts as a chemokine to recruit neutrophils
Answer: B. Promotes antiviral state in cells and activates NK cells
Explanation: IFN-α/β induce expression of antiviral proteins, reduce viral replication, and enhance NK cell activity.
Which immunodeficiency features thymic aplasia, hypocalcemia, and recurrent viral/fungal infections?
A. DiGeorge syndrome (22q11.2 deletion)
B. Wiskott–Aldrich syndrome
C. SCID
D. Ataxia–telangiectasia
Answer: A. DiGeorge syndrome (22q11.2 deletion)
Explanation: DiGeorge: failure of third/fourth pharyngeal pouch development → thymic hypoplasia/aplasia (T-cell deficiency), parathyroid hypoplasia (hypocalcemia), cardiac defects.
Which type of hypersensitivity causes serum sickness?
A. Type I
B. Type II
C. Type III
D. Type IV
Answer: C. Type III
Explanation: Serum sickness is immune-complex mediated (type III) with deposition in vessels/kidneys causing complement activation, vasculitis, fever, arthralgia.
Which receptor on macrophages binds IgG-coated bacteria to promote phagocytosis?
A. TLR4
B. FcγR (Fc gamma receptor)
C. CR1 only
D. FcεRI
Answer: B. FcγR (Fc gamma receptor)
Explanation: Fcγ receptors on phagocytes bind Fc portion of IgG (opsonization) aiding phagocytosis; complement receptors (CR1) also assist when C3b present.
Which cytokine promotes differentiation of naive CD4+ T cells into Th2 cells?
A. IL-12
B. IL-4
C. IFN-γ
D. TGF-β
Answer: B. IL-4
Explanation: IL-4 (from mast cells, basophils) drives Th2 development, promoting humoral immunity and class switching to IgE.
Which immunoglobulin is expressed on the surface of mature naive B cells?
A. Secreted IgM only
B. Membrane-bound IgM and IgD (B-cell receptor)
C. IgG only
D. IgA only
Answer: B. Membrane-bound IgM and IgD (B-cell receptor)
Explanation: Naive B cells coexpress surface IgM and IgD as B-cell receptor; after activation they secrete antibodies and can class-switch.
Which complement deficiency is associated with susceptibility to severe, recurrent pyogenic infections and autoimmunity (SLE-like disease)?
A. C3 deficiency
B. C9 deficiency only
C. C1 inhibitor deficiency
D. Properdin deficiency only
Answer: A. C3 deficiency
Explanation: C3 is central to all pathways; deficiency causes severe recurrent pyogenic infections and immune complex disease due to impaired opsonization and clearance.
Which is the immunologic basis of graft-versus-host disease (GVHD) after bone marrow transplant?
A. Host T cells attack donor tissues
B. Donor T cells recognize host MHC as foreign and attack host tissues
C. Complement-mediated destruction of graft
D. B-cell mediated rejection only
Answer: B. Donor T cells recognize host MHC as foreign and attack host tissues
Explanation: GVHD occurs when transplanted donor T cells attack recipient antigens; skin, liver, gut are commonly affected.
Which immunoglobulin deficiency is most commonly asymptomatic but can present with recurrent mucosal infections and allergy?
A. Selective IgA deficiency
B. Bruton's agammaglobulinemia
C. Severe hypogammaglobulinemia
D. Common variable immunodeficiency
Answer: A. Selective IgA deficiency
Explanation: Many are asymptomatic; others have recurrent sinopulmonary/GI infections, atopy, or anaphylaxis to IgA-containing blood products.
Which process introduces point mutations in variable regions of immunoglobulin genes to increase antibody affinity?
A. V(D)J recombination
B. Somatic hypermutation
C. Class switch recombination
D. Isotype switching
Answer: B. Somatic hypermutation
Explanation: Somatic hypermutation in germinal centers introduces nucleotide changes in V regions; selection favors higher-affinity B-cell clones.
A patient has recurrent mucocutaneous candidiasis and low IL-17 production. Which T-cell subset is likely defective?
A. Th1
B. Th2
C. Th17
D. Treg
Answer: C. Th17
Explanation: Th17 cells produce IL-17 to recruit neutrophils at mucosal sites; defects lead to chronic mucocutaneous candidiasis and extracellular fungal susceptibility.
Which molecule transports IgG across the placenta and protects IgG from catabolism?
A. FcRn (neonatal Fc receptor)
B. FcγRIIB
C. J chain
D. Poly-Ig receptor
Answer: A. FcRn (neonatal Fc receptor)
Explanation: FcRn mediates transcytosis of maternal IgG across placenta and extends IgG half-life by protecting it from degradation.
Which is an example of a type II hypersensitivity disease with functional antibody effect (not destruction)?
A. Myasthenia gravis (anti-AChR blocking)
B. Immune complex glomerulonephritis
C. Allergic asthma
D. Contact dermatitis
Answer: A. Myasthenia gravis (anti-AChR blocking)
Explanation: In MG, autoantibodies block acetylcholine receptors (functional impairment) and can also cause receptor internalization — type II autoimmune disease.
Which innate immune cell is the first responder in acute bacterial infections and is highly phagocytic?
A. Eosinophil
B. Neutrophil (polymorphonuclear leukocyte)
C. Basophil
D. Memory T cell
Answer: B. Neutrophil (polymorphonuclear leukocyte)
Explanation: Neutrophils rapidly migrate to infection sites, phagocytose pathogens, and use oxidative/non-oxidative killing mechanisms.
Which immunologic test detects specific T-cell function by measuring IFN-γ release after antigen exposure (used for latent tuberculosis)?
A. ELISA for antibodies
B. Tuberculin skin test (TST) only
C. Interferon-gamma release assay (IGRA)
D. Flow cytometry for CD4 count
Answer: C. Interferon-gamma release assay (IGRA)
Explanation: IGRA measures IFN-γ released by T cells in response to M. tuberculosis antigens; not confounded by BCG vaccination.
Which cell-surface protein is required for T-cell receptor (TCR) complex signal transduction?
A. CD28
B. CD3 complex (ζ chain)
C. CD40
D. CD19
Answer: B. CD3 complex (ζ chain)
Explanation: CD3 complex, associated with TCR, contains ITAMs for intracellular signaling after antigen recognition.
Which immunodeficiency is associated with thrombocytopenia, eczema, and recurrent infections, and is X-linked?
A. Wiskott–Aldrich syndrome
B. Ataxia–telangiectasia
C. DiGeorge syndrome
D. CVID
Answer: A. Wiskott–Aldrich syndrome
Explanation: WAS (WASP gene) causes thrombocytopenia (small platelets), eczema, and combined immunodeficiency (T and B dysfunction).
Which cytokine is central in driving acute inflammation and is an endogenous pyrogen?
A. IL-1
B. IL-10
C. IL-2
D. IL-4
Answer: A. IL-1
Explanation: IL-1 (and TNF-α) are proinflammatory cytokines causing fever, vascular permeability, and leukocyte recruitment.
Which is the principal site of B-cell activation and somatic hypermutation in secondary lymphoid organs?
A. T-cell zone of lymph node
B. Germinal centers (B-cell follicles)
C. Red pulp of spleen
D. Bone marrow only
Answer: B. Germinal centers (B-cell follicles)
Explanation: Germinal centers in follicles are where B cells proliferate, undergo somatic hypermutation and class switching with T cell help.
Which T-cell subset mediates delayed-type (type IV) hypersensitivity reactions?
A. Th1 CD4+ T cells and CD8+ T cells
B. B cells
C. Mast cells only
D. Neutrophils only
Answer: A. Th1 CD4+ T cells and CD8+ T cells
Explanation: Type IV reactions are cell-mediated by Th1 cytokines (IFN-γ) and cytotoxic T cells causing tissue damage (e.g., contact dermatitis, PPD test).
Which antibody is used in passive immunization for newborns and after exposure prophylaxis (e.g., tetanus)?
A. Live vaccine
B. Immunoglobulin (human or pooled Ig) — passive antibody
C. Inactivated vaccine only
D. Adjuvant alone
Answer: B. Immunoglobulin (human or pooled Ig) — passive antibody
Explanation: Passive immunization provides immediate short-term protection (e.g., IVIG, anti-tetanus immunoglobulin); does not induce memory.
Which molecule is most important for B-cell V(D)J recombination?
A. Activation-induced cytidine deaminase (AID)
B. RAG1/RAG2 recombinase complex
C. CD40L
D. Class II transactivator (CIITA)
Answer: B. RAG1/RAG2 recombinase complex
Explanation: RAG1/2 mediate recombination of V, D, J segments in immature B and T cells to generate antigen receptor diversity.
Which cell type expresses Toll-like receptor 9 (TLR9) that recognizes unmethylated CpG DNA?
A. B cells and plasmacytoid dendritic cells
B. RBCs
C. Neurons
D. Platelets
Answer: A. B cells and plasmacytoid dendritic cells
Explanation: TLR9 recognizes bacterial/viral unmethylated CpG DNA, triggering innate immune responses including type I interferons.
Which clinical feature suggests hyper-IgE (Job) syndrome?
A. Low IgE, recurrent viral infections
B. High IgE, eczema, recurrent staphylococcal abscesses, coarse facies
C. Thrombocytopenia and eczema
D. Absent B cells only
Answer: B. High IgE, eczema, recurrent staphylococcal abscesses, coarse facies
Explanation: Autosomal dominant STAT3 mutation → impaired Th17 differentiation, high IgE, eczema, retained primary teeth.
Which of the following is a mechanism by which tumor cells evade immune detection?
A. Upregulating MHC I expression
B. Expressing PD-L1 to inhibit T-cell function
C. Increasing costimulatory signals
D. Releasing perforin
Answer: B. Expressing PD-L1 to inhibit T-cell function
Explanation: Tumors express PD-L1 which binds PD-1 on T cells causing exhaustion/inhibition; immune checkpoint inhibitors block this interaction.
Which immunologic phenomenon explains rejection of first transplanted organ with mismatched ABO blood group?
A. Cell-mediated delayed hypersensitivity
B. Hyperacute rejection mediated by preformed anti-donor antibodies activating complement
C. Chronic rejection only
D. GVHD
Answer: B. Hyperacute rejection mediated by preformed anti-donor antibodies activating complement
Explanation: Preformed anti-donor antibodies (e.g., anti-ABO) lead to immediate complement activation, thrombosis of graft vessels, and graft loss.
Which is the major cytokine that promotes eosinophil differentiation and activation in parasitic infections and allergic diseases?
A. IL-5
B. IL-2
C. IFN-γ
D. IL-1
Answer: A. IL-5
Explanation: IL-5 (from Th2 cells) stimulates eosinophil maturation and activation, important in helminth defense and allergic inflammation.
Which immunoglobulin is most effective at fixing complement via the classical pathway?
A. IgG3 and IgM are best; IgM is extremely effective.
B. IgA only
C. IgD only
D. IgE only
Answer: A. IgG3 and IgM are best; IgM is extremely effective.
Explanation: IgM (pentamer) is highly efficient at activating complement; IgG3 is the most complement-fixing IgG subclass.
Which immune mechanism causes serum sickness–like disease after administration of foreign proteins?
A. IgE-mediated degranulation
B. Immune-complex deposition causing complement activation (type III)
C. Direct cytotoxic T-cell killing
D. NK cell-mediated ADCC
Answer: B. Immune-complex deposition causing complement activation (type III)
Explanation: Circulating immune complexes deposit in vessels/kidneys/joints, activate complement, and elicit inflammation.
Which of the following best describes affinity maturation?
A. Increased binding strength of antibody for antigen via somatic hypermutation and selection
B. Switching antibody isotype from IgM to IgG
C. Generation of naive B-cell receptor diversity via RAG enzymes
D. Addition of J chain to IgA
Answer: A. Increased binding strength of antibody for antigen via somatic hypermutation and selection
Explanation: Affinity maturation through somatic hypermutation yields B cells with higher affinity receptors selected in germinal centers.
Which condition is caused by deficiency of C1 esterase inhibitor (C1-INH)?
A. Autoimmune hemolytic anemia
B. Hereditary angioedema with episodic bradykinin-mediated swelling
C. Chronic granulomatous disease
D. Lupus
Answer: B. Hereditary angioedema with episodic bradykinin-mediated swelling
Explanation: C1-INH deficiency leads to unregulated activation of complement and kallikrein/kinin pathway → increased bradykinin → angioedema.
Which antibody type forms a pentamer and is very efficient at agglutination?
A. IgG
B. IgM
C. IgA
D. IgE
Answer: B. IgM
Explanation: IgM is pentameric (J chain) in serum and is highly multivalent, making it good for early agglutination and complement activation.
Which immune cell expresses CD56 and mediates antibody-dependent cellular cytotoxicity (ADCC)?
A. NK cell
B. Neutrophil
C. B cell
D. Plasma cell
Answer: A. NK cell
Explanation: NK cells express CD56 and FcγRIII (CD16) enabling ADCC by binding antibody-coated target cells.
Which clinical test measures antibody-mediated complement activation by detecting lysis of sheep RBCs?
A. ELISA for IgG
B. CH50 assay (classical pathway function test)
C. Nitroblue tetrazolium test
D. Flow cytometry for CD4 count
Answer: B. CH50 assay (classical pathway function test)
Explanation: CH50 measures total classical complement pathway activity via hemolysis of antibody-sensitized RBCs; low with deficiencies in early complement components.
Which interleukin is crucial for B-cell proliferation and differentiation and produced by T follicular helper (Tfh) cells?
A. IL-2
B. IL-21
C. IL-17
D. IFN-γ
Answer: B. IL-21
Explanation: IL-21 from Tfh cells promotes B-cell proliferation, plasma cell differentiation, and supports germinal center reactions.
Which of the following best explains immune checkpoint blockade therapy (e.g., anti–PD-1)?
A. Suppresses T-cell activation to reduce autoimmunity
B. Blocks inhibitory signals (PD-1/PD-L1) to restore T-cell antitumor activity
C. Depletes B cells to reduce antibody production
D. Activates complement
Answer: B. Blocks inhibitory signals (PD-1/PD-L1) to restore T-cell antitumor activity
Explanation: Anti–PD-1/PD-L1 antibodies remove inhibitory signals and unleash T cells to attack tumor cells; can cause immune-related adverse events.
Which is the major cellular component of pus?
A. Erythrocytes
B. Neutrophils
C. Macrophages only
D. Lymphocytes only
Answer: B. Neutrophils
Explanation: Acute bacterial infection → neutrophil influx and death produce purulent exudate (pus).
Which immunotherapy uses monoclonal antibodies that block TNF-α for autoimmune disease treatment?
A. Infliximab, adalimumab (anti–TNF-α)
B. Rituximab (anti-CD20)
C. Omalizumab (anti-IgE)
D. Pembrolizumab (anti–PD-1)
Answer: A. Infliximab, adalimumab (anti–TNF-α)
Explanation: Anti–TNF agents treat RA, Crohn’s disease, and other inflammatory conditions by neutralizing TNF-α, but increase risk of infections (TB reactivation).
Which immunologic test detects immune complexes by complement consumption causing hypocomplementemia in active disease?
A. Elevated CH50
B. Low C3 and C4 levels (complement consumption)
C. Increased IgE only
D. Negative ANA only
Answer: B. Low C3 and C4 levels (complement consumption)
Explanation: Immune-complex diseases (e.g., active SLE) consume complement components leading to low serum C3/C4.
Which is the main mechanism by which cytotoxic T lymphocytes kill target cells?
A. Antibody-dependent complement activation
B. Release of perforin and granzymes leading to apoptosis
C. Release of histamine
D. Phagocytosis of target cells
Answer: B. Release of perforin and granzymes leading to apoptosis
Explanation: CD8+ T cells induce apoptosis via perforin-mediated granzyme entry or Fas–FasL interactions.
Which hypersensitivity reaction underlies contact dermatitis (e.g., poison ivy)?
A. Type I
B. Type II
C. Type III
D. Type IV (delayed-type)
Answer: D. Type IV (delayed-type)
Explanation: Contact dermatitis is mediated by sensitized T cells (Th1) releasing cytokines and recruiting macrophages causing tissue injury after 48–72 hours.
Which receptor is the primary inhibitory receptor expressed by T cells targeted by cancer immunotherapy (checkpoint inhibitor)?
A. CD28
B. PD-1
C. CD40
D. CD3
Answer: B. PD-1
Explanation: PD-1 on T cells interacts with PD-L1 on tumor cells to inhibit T-cell function; blockade with antibodies restores antitumor response.
Which type of immune response is most important for controlling helminth infections?
A. Th1-mediated macrophage activation
B. Th2-mediated eosinophil activation and IgE responses
C. Th17-mediated neutrophil recruitment
D. CD8+ cytotoxic T-cell killing
Answer: B. Th2-mediated eosinophil activation and IgE responses
Explanation: Th2 cytokines (IL-4, IL-5, IL-13) promote IgE, eosinophils, and mast cell responses effective against helminths.
Which medication is used as prophylaxis in patients with complement C5 deficiency to prevent Neisseria infections?
A. Antibiotic prophylaxis and meningococcal vaccine (since complement deficiency predisposes to Neisseria)
B. Immunosuppressants
C. IVIG only
D. Antivirals
Answer: A. Antibiotic prophylaxis and meningococcal vaccine
Explanation: Patients with MAC deficiency get vaccinated (meningococcal) and may receive prophylactic antibiotics due to Neisseria susceptibility.
Which immunoglobulin is mainly found on mucosal surfaces in its secretory form?
A. Monomeric IgG
B. Dimeric secretory IgA
C. Pentameric IgM only
D. IgE only
Answer: B. Dimeric secretory IgA
Explanation: Secretory IgA (dimer with secretory component) protects mucosal surfaces by neutralizing pathogens and toxins.
Which immunodeficiency results from defective NADPH oxidase causing inability of phagocytes to generate reactive oxygen species?
A. SCID
B. Chronic granulomatous disease (CGD)
C. Bruton's agammaglobulinemia
D. DiGeorge syndrome
Answer: B. Chronic granulomatous disease (CGD)
Explanation: NADPH oxidase defect → impaired respiratory burst → infections with catalase-positive organisms and granuloma formation.
Which cytokine is primarily anti-inflammatory and produced by regulatory T cells?
A. IL-1
B. IL-10
C. TNF-α
D. IFN-γ
Answer: B. IL-10
Explanation: IL-10 suppresses macrophage and Th1 responses and promotes tolerance; produced by Tregs and some macrophages.
Which is the major adhesion molecule pair mediating leukocyte extravasation (firm adhesion) to endothelium?
A. Selectins only
B. LFA-1 (integrin) on leukocyte binding ICAM-1 on endothelium
C. Fc receptors
D. T-cell receptors
Answer: B. LFA-1 (integrin) on leukocyte binding ICAM-1 on endothelium
Explanation: Rolling mediated by selectins, activation by chemokines, then integrin-mediated firm adhesion (LFA-1–ICAM-1) and transmigration.
Which immunoglobulin is typically elevated in parasitic infections and allergic conditions?
A. IgG only
B. IgE
C. IgM only
D. IgD only
Answer: B. IgE
Explanation: IgE binds parasites and mediates eosinophil activation via Fc receptors; elevated in allergic diseases.
Which test differentiates between deficiencies of early classical complement components (C1–C4) and terminal components (C5–C9)?
A. ELISA for IgG
B. CH50 assay (classical) and AH50 (alternative) with specific complement levels measurement
C. NBT test
D. ANA titer only
Answer: B. CH50 assay (classical) and AH50 (alternative) with specific complement levels measurement
Explanation: CH50 assesses classical pathway (C1–C9); absent CH50 with normal individual C levels suggests terminal deficiency; specific C assays localize defect.
Which immunodeficiency shows increased risk of severe pyogenic infections, low IgG, and poor response to vaccines, but normal B-cell numbers?
A. Common variable immunodeficiency (CVID)
B. Bruton's agammaglobulinemia
C. Selective IgA deficiency
D. SCID
Answer: A. Common variable immunodeficiency (CVID)
Explanation: CVID has impaired B-cell differentiation to plasma cells → low immunoglobulins and poor vaccine responses; variable onset.
Which viral infection is classically associated with triggering Guillain–Barré syndrome by molecular mimicry?
A. Epstein–Barr virus
B. Campylobacter jejuni (bacterial) — but viruses like CMV can also trigger GBS
C. Hepatitis B only
D. Varicella zoster only
Answer: B. Campylobacter jejuni (bacterial) — but viruses like CMV can also trigger GBS
Explanation: GBS often follows infections (C. jejuni, CMV, EBV), where immune response cross-reacts with peripheral nerve myelin (molecular mimicry).
Which immunologic phenomenon explains development of autoimmunity when central tolerance fails and peripheral mechanisms are insufficient?
A. Molecular mimicry, epitope spreading, bystander activation, failure of Tregs
B. Passive immunity only
C. Complement activation only
D. Antibody-dependent cellular cytotoxicity only
Answer: A. Molecular mimicry, epitope spreading, bystander activation, failure of Tregs
Explanation: Autoimmunity arises from multiple mechanisms including cross-reactive immune responses to pathogens, exposure of hidden antigens, and regulatory defects.
Which vaccine adjuvant commonly enhances immune response by creating a depot for antigen and activating innate immunity?
A. Aluminum salts (alum)
B. Live attenuated virus
C. Recombinant protein alone without adjuvant
D. Antibiotic
Answer: A. Aluminum salts (alum)
Explanation: Alum is a classic adjuvant forming antigen depot and enhancing uptake by APCs and Th2-skewed responses; many vaccines use adjuvants to boost immunogenicity.