Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 191: Phagocytosis is enhanced when bacteria are coated with complement and Ig. What mechanism best describes this enhanced phagocytosis?

A. Receptor-mediated endocytosis
B. Pseudopod formation
C. Myeloperoxidase-mediated destruction
D. C3b and Fc receptor-mediated phagocytosis (Correct Answer)

Explanation: ### Explanation **Correct Option: D (C3b and Fc receptor-mediated phagocytosis)** The process described in the question is **Opsonization**. Opsonization is the "coating" of a pathogen with specific proteins (opsonins) to make it more "palatable" to phagocytes (neutrophils and macrophages). * **Mechanism:** The two most important opsonins are **C3b** (from the complement system) and **IgG** (specifically the Fc portion). * Phagocytes possess specific surface receptors: **CR1** (for C3b) and **FcγR** (for the Fc portion of IgG). When these receptors bind to their respective ligands on the bacterial surface, it triggers a "zipper-like" engulfment, significantly increasing the efficiency of phagocytosis compared to non-opsonized bacteria. --- ### Why Other Options are Incorrect: * **A. Receptor-mediated endocytosis:** While phagocytosis is a form of endocytosis, this term usually refers to the internalisation of small molecules (like LDL or iron) via clathrin-coated pits, rather than the engulfment of large particulate matter like bacteria. * **B. Pseudopod formation:** This is a *structural step* of phagocytosis where the cell membrane extends around the particle. It is a consequence of the signaling triggered by opsonin-receptor binding, not the mechanism of enhancement itself. * **C. Myeloperoxidase-mediated destruction:** This refers to the **intracellular killing** phase (oxidative burst) that occurs *after* the bacteria have been ingested into the phagolysosome. It does not facilitate the initial attachment or engulfment. --- ### NEET-PG High-Yield Pearls: * **Most potent opsonins:** IgG and C3b. (Mnemonic: **I**g**G** and **C3b** **G**et **B**acteria). * **Acute phase reactant opsonin:** C-reactive protein (CRP) and Mannose-binding lectin (MBL) also act as opsonins. * **Deficiency:** Defects in opsonization (e.g., C3 deficiency) lead to recurrent infections with **encapsulated bacteria** (e.g., *S. pneumoniae, H. influenzae*). * **Receptor:** The Fc receptor involved in opsonization is specifically for **IgG**; IgM is a poor opsonin directly because phagocytes lack receptors for the Fc portion of IgM.

Question 192: Immunity acquired due to the injection of immunologically competent lymphocytes is termed as?

A. Innate immunity
B. Adoptive immunity (Correct Answer)
C. Active immunity
D. Local immunity

Explanation: ### Explanation **Correct Answer: B. Adoptive immunity** **Why it is correct:** Adoptive immunity is a specialized form of passive immunity where **immunologically competent cells** (such as T-lymphocytes or sensitized lymphocytes) are transferred from a donor to a recipient. Unlike standard passive immunity, which involves the transfer of pre-formed antibodies (proteins), adoptive immunity involves the transfer of **living cells** that can continue to function and mount an immune response within the host. This is commonly utilized in cancer immunotherapy (e.g., CAR-T cell therapy) and in treating certain intracellular infections or immunodeficiency states where the patient's own cellular immunity is compromised. **Why the other options are incorrect:** * **A. Innate immunity:** This is the non-specific, first line of defense present from birth (e.g., skin, mucosal barriers, phagocytes). It does not require prior exposure or the transfer of sensitized lymphocytes. * **C. Active immunity:** This occurs when the individual’s own immune system is stimulated to produce antibodies and memory cells following exposure to an antigen (either via natural infection or vaccination). It takes time to develop but is long-lasting. * **D. Local immunity:** This refers to immune responses localized to specific sites, primarily mediated by Secretory IgA (sIgA) at mucosal surfaces (e.g., gut or respiratory tract). **High-Yield NEET-PG Pearls:** * **Passive Immunity:** Provides immediate but temporary protection. It does not trigger the recipient's immune system or create memory. * **Adoptive Transfer:** The classic example is the transfer of **tuberculin sensitivity** via lymphocytes, which cannot be transferred via serum/antibodies. * **Key Distinction:** If you transfer **Serum**, it is Passive Immunity. If you transfer **Cells**, it is Adoptive Immunity.

Question 193: Decreased T cell immunity is a feature of which of the following conditions?

A. DiGeorge syndrome (Correct Answer)
B. Hyper IgM syndrome
C. Severe congenital neutropenia
D. Chronic granulomatous disease

Explanation: **Explanation:** **DiGeorge Syndrome (Correct Answer):** DiGeorge syndrome (22q11.2 deletion) is caused by the failure of the **3rd and 4th pharyngeal pouches** to develop. This leads to **thymic hypoplasia or aplasia**, resulting in a deficiency of mature T cells. Since the thymus is the primary site for T-cell maturation and "education," its absence leads to profound defects in cell-mediated immunity, making patients susceptible to viral, fungal, and protozoal infections. **Analysis of Incorrect Options:** * **Hyper IgM Syndrome:** This is primarily a **humoral (B-cell) immunity defect** caused by a mutation in the CD40 ligand. While it involves T-cell signaling, the hallmark is the inability of B cells to undergo class switching, leading to high IgM but low IgG, IgA, and IgE. * **Severe Congenital Neutropenia (Kostmann Syndrome):** This is a **phagocytic defect** characterized by a maturation arrest of neutrophils in the bone marrow, leading to profound neutropenia. T-cell function remains intact. * **Chronic Granulomatous Disease (CGD):** This is a **phagocytic dysfunction** caused by a defect in the NADPH oxidase enzyme. It impairs the "respiratory burst," preventing neutrophils from killing catalase-positive organisms. T-cell immunity is not primarily affected. **NEET-PG High-Yield Pearls:** * **CATCH-22 Mnemonic for DiGeorge:** **C**ardiac defects (Truncus arteriosus/TOF), **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia (due to parathyroid hypoplasia). * **Radiology Sign:** Look for the **absence of a thymic shadow** on a newborn’s chest X-ray. * **NBT Test/DHR Flow Cytometry:** Used to diagnose CGD, not T-cell defects. * **Delayed Type Hypersensitivity (DTH):** Skin tests (like the Mantoux test) are often negative (anergy) in DiGeorge syndrome due to T-cell deficiency.

Question 194: Which part of the immunoglobulin molecule determines its class?

A. Heavy chain (Correct Answer)
B. Light chain
C. Both heavy and light chains
D. Neither heavy nor light chain

Explanation: ### Explanation **1. Why the Heavy Chain is Correct:** The classification of immunoglobulins (IgG, IgA, IgM, IgE, and IgD) is determined solely by the **Heavy (H) chain** type. There are five distinct types of heavy chains, designated by Greek letters: **gamma (γ)** for IgG, **alpha (α)** for IgA, **mu (μ)** for IgM, **epsilon (ε)** for IgE, and **delta (δ)** for IgD. These chains differ in their amino acid sequences and structural properties (such as the number of constant domains and hinge regions), which dictate the molecule's biological activity and effector functions. **2. Why Other Options are Incorrect:** * **Light Chain:** While light chains are essential components of the antibody, they do not determine the class. There are only two types of light chains—**Kappa (κ) and Lambda (λ)**. Any class of immunoglobulin can have either kappa or lambda light chains, but never both in a single molecule. * **Both Heavy and Light Chains:** The class is defined by the heavy chain alone. The light chain contributes to the antigen-binding site (Fab) but not to the isotype classification. * **Neither:** This is incorrect as the structural identity of the heavy chain is the fundamental basis for isotype categorization. **3. NEET-PG High-Yield Pearls:** * **Isotype:** Determined by the Heavy chain (defines the class). * **Allotype:** Determined by genetic variations within the same class among different individuals. * **Idiotype:** Determined by the variable regions (antigen-binding specificity). * **Valency:** IgM is a pentamer (valency of 10), while IgA is typically a dimer in secretions (valency of 4). * **Placental Transfer:** Only **IgG** can cross the placenta (specifically via the FcRn receptor). * **First Antibody:** **IgM** is the first antibody produced in a primary immune response.

Question 195: All of the following compounds are mitogens that stimulate human T cells to proliferate, EXCEPT:

A. Lipopolysaccharide (Correct Answer)
B. Concanavalin A
C. Anti CD3 antibody
D. Phytohemagglutinin

Explanation: **Explanation:** Mitogens are substances that induce mitosis (cell division) in lymphocytes in a non-specific, polyclonal manner, regardless of their antigen specificity. **1. Why Lipopolysaccharide (LPS) is the correct answer:** LPS (Endotoxin), derived from the cell wall of Gram-negative bacteria, is a potent **B-cell mitogen** in humans. It does not stimulate T-cell proliferation. It acts by binding to Toll-like receptor 4 (TLR4) on B-cells, leading to their activation and polyclonal antibody production. **2. Analysis of Incorrect Options (T-cell Mitogens):** * **Phytohemagglutinin (PHA):** A lectin derived from kidney beans; it is a classic, potent stimulator of **T-cells**. * **Concanavalin A (ConA):** A lectin derived from jack beans; it specifically stimulates **T-cells**. * **Anti-CD3 Antibody:** CD3 is a core component of the T-cell receptor (TCR) complex. Antibodies against CD3 mimic the signal of an antigen, leading to robust, polyclonal **T-cell** activation. **3. High-Yield Clinical Pearls for NEET-PG:** * **T-cell Mitogens:** PHA, ConA, and Anti-CD3. * **B-cell Mitogens:** LPS, Epstein-Barr Virus (EBV), and Staphylococcus aureus Cowan I strain (SAC). * **Pokeweed Mitogen (PWM):** Unique because it stimulates **both** T-cells and B-cells. * **Clinical Use:** Mitogen stimulation tests are used in clinical immunology to assess the functional integrity of a patient’s cellular (T-cell) or humoral (B-cell) immunity, such as in suspected Primary Immunodeficiency Disorders (PIDs).

Question 196: Recurrent Neisseria infections are not predisposed by which of the following?

A. Early complement component deficiency (Correct Answer)
B. Late complement component deficiency
C. Factor D deficiency
D. Properdin deficiency

Explanation: To understand the predisposition to recurrent *Neisseria* infections, one must focus on the **Membrane Attack Complex (MAC)**, which is essential for the lysis of thin-walled bacteria like *Neisseria meningitidis* and *Neisseria gonorrhoeae*. ### **Why "Early Complement Component Deficiency" is the Correct Answer** Deficiencies in early components of the **Classical Pathway (C1, C2, C4)** primarily predispose individuals to **immune-complex diseases** (like SLE) and infections with **encapsulated bacteria** (e.g., *S. pneumoniae*, *H. influenzae*) due to impaired opsonization. While C3 deficiency is severe and can lead to *Neisseria* infections, the "early components" (C1, C2, C4) are generally not specifically associated with recurrent Neisserial outbreaks. ### **Analysis of Incorrect Options** * **Late Complement Component Deficiency (C5–C9):** These components form the MAC. Deficiency in any of these (especially C5, C6, C7, or C8) is the classic risk factor for recurrent disseminated Neisserial infections because the body cannot physically puncture the bacterial cell wall. * **Factor D and Properdin Deficiency:** These are essential components of the **Alternative Pathway**. Properdin stabilizes the C3 convertase. Since the alternative pathway is a major amplification loop for MAC formation, deficiencies in Factor D or Properdin significantly increase susceptibility to *Neisseria*. ### **High-Yield Clinical Pearls for NEET-PG** * **MAC Deficiency (C5-C9):** Most strongly associated with *Neisseria* (1,000 to 10,000-fold increased risk). * **Properdin Deficiency:** An **X-linked** inheritance pattern; suspect this in a male child with fulminant meningococcemia. * **C3 Deficiency:** The most severe complement deficiency, leading to recurrent pyogenic infections and Type II Hypersensitivity (Membranoproliferative Glomerulonephritis). * **CH50 Assay:** Used to screen for classical pathway deficiencies; **AH50** screens the alternative pathway.

Question 197: A child has a history of recurrent infections with organisms having polysaccharide antigens (i.e., Streptococcus pneumoniae and Haemophilus influenzae). This susceptibility can be explained by a deficiency of?

A. C3 nephritic factor
B. C5
C. IgG subclass 2 (Correct Answer)
D. Myeloperoxidase in phagocytic cells

Explanation: **Explanation:** **Why IgG subclass 2 is correct:** Immunoglobulin G (IgG) is divided into four subclasses (IgG1–IgG4). **IgG2** is the primary antibody responsible for the immune response against **encapsulated bacteria** (e.g., *S. pneumoniae*, *H. influenzae type b*, and *N. meningitidis*). These bacteria possess **polysaccharide capsules** that are T-cell independent antigens. While IgG1 and IgG3 typically respond to protein antigens, IgG2 is specifically specialized for carbohydrate/polysaccharide antigens. Therefore, a selective IgG2 deficiency leads to recurrent sinopulmonary infections with encapsulated organisms, even if total IgG levels appear near normal. **Analysis of Incorrect Options:** * **A. C3 nephritic factor:** This is an autoantibody that stabilizes C3 convertase, leading to continuous C3 consumption. It is associated with Type II Membranoproliferative Glomerulonephritis (MPGN) and partial lipodystrophy, not specific susceptibility to polysaccharide antigens. * **B. C5:** Deficiency of late complement components (C5–C9) specifically predisposes individuals to recurrent **Neisserial infections** (Meningitis and Gonorrhea) due to failure of the Membrane Attack Complex (MAC) formation. * **D. Myeloperoxidase (MPO):** MPO deficiency in phagocytes leads to impaired production of hypochlorous acid. While often asymptomatic, it primarily predisposes patients to disseminated **Candidiasis**, not specifically to encapsulated bacteria. **High-Yield Clinical Pearls for NEET-PG:** * **IgG1:** Most abundant subclass; responds to protein antigens (e.g., Tetanus toxoid). * **IgG2:** Responds to polysaccharide antigens; deficiency is the most common subclass deficiency in children. * **IgG3:** Most effective at activating complement. * **IgG4:** Associated with chronic allergen exposure and IgG4-related systemic diseases. * **Wiskott-Aldrich Syndrome:** Often shows low IgG2 levels along with low IgM and high IgA/IgE.

Question 198: All of the following are true regarding Bruton's Agammaglobulinemia except:

A. It is X-linked. (Correct Answer)
B. T cell abnormality is seen.
C. It is seen only in males.
D. There is an increase in the number of plasma cells.

Explanation: **Explanation:** Bruton’s Agammaglobulinemia, also known as **X-linked Agammaglobulinemia (XLA)**, is a primary immunodeficiency caused by a mutation in the **BTK (Bruton Tyrosine Kinase) gene**. This kinase is essential for the maturation of Pre-B cells into mature B cells. **Why Option D is the correct answer (the "Except" statement):** In XLA, there is a complete failure of B-cell maturation. Consequently, there are **virtually no mature B cells** in the peripheral blood and a **marked absence of plasma cells** in lymphoid tissues. Since plasma cells are responsible for antibody production, all classes of immunoglobulins (IgG, IgA, IgM, IgE, IgD) are severely depleted. **Analysis of other options:** * **Option A & C:** XLA follows an **X-linked recessive** inheritance pattern. Therefore, it is typically seen **only in males**, while females act as asymptomatic carriers. * **Option B:** This is a pure B-cell defect. **T-cell numbers and functions remain normal**, which is a key diagnostic feature used to differentiate it from Combined Immunodeficiencies (like SCID). **NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Recurrent pyogenic infections (e.g., *S. pneumoniae*, *H. influenzae*) starting after 6 months of age (once maternal IgG wanes). * **Physical Exam:** Characterized by **absent or hypoplastic tonsils** and lymph nodes. * **Diagnosis:** Flow cytometry shows absent CD19+ B cells; Quantitative PCR confirms BTK gene mutation. * **Treatment:** Lifelong Intravenous Immunoglobulin (IVIG) replacement; Live vaccines are strictly contraindicated.

Question 199: The Weil-Felix reaction is a heterophile antibody reaction due to sharing of Rickettsial antigen with which of the following organisms?

A. Shigella
B. Proteus (Correct Answer)
C. Chlamydia
D. Mycoplasma

Explanation: **Explanation:** The **Weil-Felix reaction** is a classic example of a **heterophile antibody reaction**. It is based on the principle of **cross-reactivity**, where antibodies produced against certain Rickettsial antigens react with specific strains of **Proteus vulgaris (OX-19, OX-2)** and **Proteus mirabilis (OX-K)**. This occurs because these organisms share common alkali-stable carbohydrate antigens. * **Why Proteus is correct:** In Rickettsial infections (except Q fever), the body produces antibodies that agglutinate specific Proteus antigens. * **OX-19 and OX-2:** React with antibodies from the Typhus group and Spotted Fever group. * **OX-K:** Reacts with antibodies from Scrub Typhus (*Orientia tsutsugamushi*). **Analysis of Incorrect Options:** * **A. Shigella:** Causes bacillary dysentery; it does not share antigenic determinants with Rickettsia. * **C. Chlamydia:** These are obligate intracellular bacteria, but they are diagnosed via NAAT, Giemsa stain, or serology (MIF), not through Proteus cross-reactivity. * **D. Mycoplasma:** Associated with **Cold Agglutinin disease** (autoantibodies against RBC I-antigens), which is a different type of heterophile reaction. **High-Yield Clinical Pearls for NEET-PG:** * **Negative Weil-Felix:** Q fever (*Coxiella burnetii*) and Rickettsialpox (*R. akari*) do **not** show a positive Weil-Felix reaction. * **Gold Standard:** The Indirect Fluorescent Antibody (IFA) test has replaced Weil-Felix in modern practice due to the latter's low sensitivity and specificity. * **Scrub Typhus:** Specifically associated with the **OX-K** strain.

Question 200: Which of the following is NOT a type-II hypersensitivity reaction?

A. Hemorrhagic disease of the newborn
B. Graves disease
C. Rheumatoid arthritis (Correct Answer)
D. Hemolytic anemia

Explanation: **Explanation:** Hypersensitivity reactions are classified based on the immune mechanism involved. **Type II Hypersensitivity** (Cytotoxic) involves IgG or IgM antibodies directed against antigens on specific cell surfaces or tissues, leading to cell destruction, inflammation, or cellular dysfunction. **Why Rheumatoid Arthritis (RA) is the correct answer:** Rheumatoid Arthritis is primarily a **Type III Hypersensitivity** reaction. It involves the formation of immune complexes (e.g., Rheumatoid Factor, which is an IgM antibody against the Fc portion of IgG). These complexes deposit in the synovial joints, triggering a complement-mediated inflammatory response. It also has a significant **Type IV** (cell-mediated) component involving T-cells and cytokines like TNF-alpha. **Analysis of Incorrect Options (Type II Reactions):** * **Hemorrhagic disease of the newborn (HDN):** Also known as Erythroblastosis Fetalis. Maternal IgG antibodies cross the placenta and destroy fetal RBCs (antigen-antibody reaction on cell surface). * **Graves’ Disease:** A specific subtype of Type II (Type V/Stimulatory). Antibodies (TSI) bind to TSH receptors on thyroid cells, stimulating overproduction of thyroid hormones. * **Hemolytic Anemia:** Autoimmune hemolytic anemia involves antibodies binding directly to RBC membranes, leading to their destruction via the complement system or splenic macrophages. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Types:** **ACID** (Type I: **A**naphylactic/Atopic; Type II: **C**ytotoxic; Type III: **I**mmune Complex; Type IV: **D**elayed). * **Type II Examples:** Myasthenia Gravis, Goodpasture Syndrome, Rheumatic Fever, and Pemphigus Vulgaris. * **Type III Examples:** SLE, Post-streptococcal glomerulonephritis (PSGN), and Arthus reaction. * **Key Distinction:** If the antigen is **soluble** and forms a complex, it is Type III; if the antigen is **fixed** on a cell/tissue, it is Type II.

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Immunology — MCQs

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