Immunology — MCQs

A 1-year-old boy is brought to the OPD with complaints of inability to gain weight and chronic diarrhea. He was growing well until 6 months of age, after which he started developing recurrent episodes of pneumonia. Family history is positive for similar symptoms in a maternal uncle. On examination, he is below the 3rd percentile for weight. Tonsils are absent. Stool is positive for Giardia. Which of the following is not true regarding his condition?

Q618Easy

What is the central component of the complement pathway?

Q619Easy

DiGeorge syndrome is characterized by a deficiency of which of the following?

Q620Easy

Which bacterium is known to produce superantigens?

Immunology Indian Medical PG Practice Questions and MCQs

Question 611: Which of the following inhibits the activation of the C3 complement pathway?

A. CD 59
B. CD 55 (Correct Answer)
C. Factor D
D. Factor E

Explanation: **Explanation:** The complement system is a tightly regulated cascade of proteins. To prevent damage to host cells, the body uses regulatory proteins to inhibit spontaneous or excessive activation. **Why CD 55 is correct:** **CD 55**, also known as **Decay-Accelerating Factor (DAF)**, is a membrane-bound protein that inhibits the C3 complement pathway. It functions by binding to the **C3 convertase** (C4b2a in the classical pathway and C3bBb in the alternative pathway) and accelerating its dissociation (decay). By destabilizing the C3 convertase, CD 55 prevents the cleavage of C3 into C3a and C3b, effectively halting the cascade at its most critical amplification step. **Analysis of Incorrect Options:** * **CD 59 (Protectin):** This protein acts much later in the cascade. It inhibits the formation of the **Membrane Attack Complex (MAC)** by preventing the incorporation of C9 into the C5b-8 complex. It does not inhibit C3 activation. * **Factor D:** This is a serine protease essential for the **activation** of the alternative pathway. It cleaves Factor B into Ba and Bb; therefore, it promotes rather than inhibits the pathway. * **Factor E:** This is not a recognized component or regulator of the human complement system. **Clinical Pearls for NEET-PG:** * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** This condition is caused by a deficiency of GPI-anchored proteins, specifically **CD 55 and CD 59**. Without these regulators, red blood cells are susceptible to spontaneous complement-mediated lysis, leading to intravascular hemolysis. * **Diagnosis of PNH:** Flow cytometry showing the absence of CD 55/CD 59 on RBCs/WBCs is the gold standard. * **C3 Convertase:** The "central hub" of all three complement pathways (Classical, Alternative, and Lectin).

Question 612: Deficiency of which complement system components is associated with Neisseria meningitis infections?

A. C1-C4
B. C5-C9 (Correct Answer)
C. C3
D. C2

Explanation: **Explanation:** The complement system is a vital component of innate immunity. The correct answer is **C5-C9** because these components form the **Membrane Attack Complex (MAC)**. 1. **Why C5-C9 is Correct:** The MAC (C5b, C6, C7, C8, and C9) is responsible for creating pores in the cell membranes of Gram-negative bacteria, leading to osmotic lysis. *Neisseria* species (both *N. meningitidis* and *N. gonorrhoeae*) have thin peptidoglycan layers and are uniquely susceptible to MAC-mediated killing. Patients with deficiencies in these "terminal" complement components have a **1,000 to 10,000-fold increased risk** of recurrent systemic neisserial infections. 2. **Why Other Options are Incorrect:** * **C1, C2, C4 (Options A & D):** These are early components of the Classical Pathway. Deficiencies here typically present with **Immune Complex diseases** (like Systemic Lupus Erythematosus - SLE) because they are essential for clearing apoptotic debris and immune complexes. While C2 deficiency is the most common complement deficiency, it rarely leads to isolated *Neisseria* susceptibility. * **C3 (Option C):** C3 is the "central hub" where all pathways converge. Deficiency of C3 is the most severe, leading to recurrent infections with **encapsulated bacteria** (e.g., *S. pneumoniae*, *H. influenzae*) due to failed opsonization, but it is not specifically linked to *Neisseria* alone. **High-Yield Clinical Pearls for NEET-PG:** * **CH50 Assay:** Used to screen for deficiencies in the classical and terminal pathways. * **Properdin Deficiency:** An X-linked condition (Alternative pathway) that also increases susceptibility to *Neisseria*. * **Eculizumab:** A monoclonal antibody against C5 (used in PNH) mimics a C5 deficiency, requiring patients to be vaccinated against *Meningococcus* before starting therapy.

Question 613: Elevated IgG and IgM antibody titers to parvovirus suggest a diagnosis of?

A. Fifth disease (Correct Answer)
B. Susceptibility to chickenpox
C. Possible subacute sclerosing panencephalitis (SSPE)
D. Possible hepatitis B infection

Explanation: **Explanation:** The presence of elevated **IgM and IgG** antibodies to Parvovirus B19 is diagnostic of a recent or acute infection. **IgM** indicates an acute phase (appearing within days of infection), while **IgG** appears shortly after and signifies developing immunity. **Parvovirus B19** is the causative agent of **Fifth disease** (Erythema Infectiosum). * **Why Option A is correct:** Fifth disease typically presents in children with a characteristic "slapped-cheek" rash followed by a reticular (lace-like) rash on the trunk and limbs. In adults, it often manifests as acute polyarthritis. * **Why Option B is incorrect:** Susceptibility to chickenpox (Varicella-Zoster Virus) would be indicated by a *lack* of IgG antibodies. Active infection would show VZV-specific IgM. * **Why Option C is incorrect:** SSPE is a rare, progressive neurological complication of **Measles** virus, characterized by high titers of anti-measles antibodies in the CSF and serum, not parvovirus. * **Why Option D is incorrect:** Hepatitis B diagnosis relies on specific markers like HBsAg, anti-HBc, and HBeAg. Parvovirus is not hepatotropic in the same manner. **High-Yield Clinical Pearls for NEET-PG:** 1. **Aplastic Crisis:** Parvovirus B19 infects and lyses **erythroid progenitor cells**. In patients with high RBC turnover (e.g., Sickle Cell Anemia, Hereditary Spherocytosis), it can cause a life-threatening transient aplastic crisis. 2. **Hydrops Fetalis:** In pregnant women, parvovirus can cross the placenta, leading to severe fetal anemia, high-output cardiac failure, and hydrops fetalis. 3. **Receptor:** The virus binds to the **P-antigen** (globoside) on erythroblasts. 4. **Morphology:** It is the smallest DNA virus, non-enveloped, and notably **single-stranded (ssDNA)**.

Question 614: AIDS is a disease of the immune system primarily affecting which cells?

A. Granulocytes
B. Immunoglobulins
C. Opsonins
D. T Lymphocytes (Correct Answer)

Explanation: **Explanation:** The Human Immunodeficiency Virus (HIV) specifically targets cells expressing the **CD4 receptor** on their surface. The primary target is the **CD4+ T lymphocyte** (Helper T cell). HIV uses its surface glycoprotein **gp120** to bind to the CD4 molecule, leading to the progressive depletion of these cells. Since CD4+ T cells are the "master regulators" of the immune response, their loss results in profound immunosuppression, making the patient susceptible to opportunistic infections and malignancies. **Analysis of Incorrect Options:** * **A. Granulocytes:** These are part of the innate immune system (neutrophils, eosinophils, basophils). While their function may be indirectly impaired in advanced AIDS, they are not the primary target of the virus. * **B. Immunoglobulins:** These are antibodies produced by B cells. In AIDS, B cell function is dysregulated (often causing polyclonal hypergammaglobulinemia), but the disease is defined by cellular deficiency, not a primary lack of immunoglobulins. * **C. Opsonins:** These are molecules (like C3b or IgG) that coat pathogens to facilitate phagocytosis. They are proteins, not cells, and are not directly targeted by HIV. **High-Yield Clinical Pearls for NEET-PG:** * **The Hallmark of AIDS:** A CD4+ T cell count **<200 cells/mm³** (Normal: 500–1500 cells/mm³). * **Coreceptors:** HIV also requires chemokine coreceptors for entry: **CCR5** (found on macrophages/T cells, important in early infection) and **CXCR4** (found on T cells, associated with late-stage progression). * **Inversion of Ratio:** In AIDS, the normal CD4:CD8 ratio (typically 2:1) is **inverted** (less than 1:1). * **Other Targets:** HIV also infects macrophages and dendritic cells, which act as reservoirs for the virus.

Question 615: What is the earliest immunoglobulin synthesized by the fetus?

A. IgA
B. IgG
C. IgE
D. IgM (Correct Answer)

Explanation: **Explanation:** The correct answer is **IgM**. **Why IgM is correct:** Immunoglobulin M (IgM) is the first antibody class to be synthesized by the fetus, beginning around the **20th week of intrauterine life**. Because IgM is a large pentameric molecule, it cannot cross the placental barrier. Therefore, the presence of specific IgM antibodies in a neonate’s serum is a definitive diagnostic marker for **congenital infections** (e.g., TORCH infections), as it indicates an active fetal immune response rather than maternal transfer. **Why the other options are incorrect:** * **IgG:** While IgG is the most abundant immunoglobulin in the fetus, it is **not synthesized** by the fetus in significant amounts initially. Instead, it is actively transported across the placenta from the mother (starting at 12 weeks) to provide passive immunity. * **IgA:** This is primarily a secretory antibody. Fetal synthesis of IgA begins much later (around 30 weeks) and levels remain very low at birth. It is primarily acquired postnatally through colostrum and breast milk. * **IgE:** This is involved in type I hypersensitivity and parasitic infections. It is produced in negligible amounts by the fetus and does not cross the placenta. **High-Yield Clinical Pearls for NEET-PG:** * **Order of synthesis:** IgM is the first to be synthesized, followed by IgG and then IgA. * **Placental Transfer:** **IgG** is the *only* immunoglobulin that crosses the placenta (via neonatal Fc receptors). * **Adult levels:** IgG reaches adult levels by 5–8 years, while IgM reaches adult levels by 1 year of age. * **Colostrum:** Rich in **Secretory IgA**, providing local mucosal immunity to the neonate’s gut.

Question 616: Prozone phenomenon is due to which of the following?

A. Excess antigen
B. Excess antibody (Correct Answer)
C. Hyperimmune reaction
D. Disproportionate antigen-antibody cells

Explanation: ### Explanation The **Prozone phenomenon** is a false-negative serological result that occurs when the concentration of antibodies is so high that it prevents the formation of a stable antigen-antibody lattice. #### 1. Why "Excess Antibody" is Correct For a visible reaction (like precipitation or agglutination) to occur, antibodies and antigens must be in a **Zone of Equivalence**, where they form a large, cross-linked lattice. In the **Prozone**, there is an **excess of antibodies**. Each antigenic determinant is quickly saturated by a single antibody molecule, preventing the antibodies from "bridging" between two different antigens. Since no lattice forms, no visible reaction occurs, leading to a false-negative result despite the presence of specific antibodies. #### 2. Analysis of Incorrect Options * **A. Excess Antigen:** This leads to the **Post-zone phenomenon**. Here, every antibody binding site is saturated by an excess of free antigens, again preventing lattice formation. * **C. Hyperimmune reaction:** This is a clinical state of exaggerated immune response (like anaphylaxis) and is not a laboratory term for titration errors. * **D. Disproportionate antigen-antibody cells:** This is a vague descriptor. The phenomenon specifically relates to the concentration of soluble or particulate molecules, not "cells." #### 3. NEET-PG High-Yield Pearls * **Clinical Significance:** Prozone is most famously associated with **Secondary Syphilis** (VDRL/RPR tests) and **Brucellosis**. If a clinician strongly suspects these diseases but the test is negative, the serum should be **diluted** to reach the zone of equivalence. * **Marrack’s Lattice Hypothesis:** This is the underlying principle explaining that optimal precipitation occurs when the ratio of antigen to antibody is equivalent. * **Key takeaway:** If a test is negative but the clinical suspicion is high, **dilute the serum** to eliminate the Prozone effect.

Question 617: A 1-year-old boy is brought to the OPD with complaints of inability to gain weight and chronic diarrhea. He was growing well until 6 months of age, after which he started developing recurrent episodes of pneumonia. Family history is positive for similar symptoms in a maternal uncle. On examination, he is below the 3rd percentile for weight. Tonsils are absent. Stool is positive for Giardia. Which of the following is not true regarding his condition?

A. All classes of immunoglobulin levels are reduced
B. Lymph node biopsy shows depletion of follicles
C. Both humoral and cell-mediated immunity are affected (Correct Answer)
D. It is caused by a mutation of the Bruton's tyrosine kinase (Btk) gene

Explanation: **Explanation:** The clinical presentation—a male infant, onset of symptoms after 6 months (when maternal IgG wanes), recurrent pyogenic infections (pneumonia), absent tonsils, and a positive family history in a maternal uncle (X-linked inheritance)—points directly to **X-linked Agammaglobulinemia (XLA)**, also known as **Bruton’s Agammaglobulinemia**. **1. Why Option C is the correct answer (The "Not True" statement):** In XLA, the defect is specifically in **humoral immunity**. The mutation in the **Btk gene** prevents pre-B cells from maturing into B cells. However, **T-cell mediated immunity remains intact**. Patients can handle most viral and fungal infections normally, though they are susceptible to certain enteroviruses and *Giardia* (due to lack of secretory IgA). **2. Analysis of Incorrect Options:** * **Option A:** True. Since B-cell maturation is arrested, there is a profound deficiency of all classes of immunoglobulins (IgG, IgA, IgM, IgE, and IgD). * **Option B:** True. Lymph nodes in XLA lack **germinal centers and follicles**, as these areas are primarily composed of B-cells. Similarly, tonsils and Peyer's patches are atrophic or absent. * **Option D:** True. The condition is caused by a mutation in the **Bruton’s tyrosine kinase (Btk)** gene located on the X chromosome (Xq21.3-22). **Clinical Pearls for NEET-PG:** * **Classic Triad:** Male infant + Recurrent pyogenic infections after 6 months + Absent B-cells in peripheral blood. * **Common Pathogens:** *S. pneumoniae, H. influenzae* (respiratory) and *Giardia lamblia* (GI tract). * **Diagnosis:** Flow cytometry showing absent or <2% CD19+ B-cells. * **Treatment:** Intravenous Immunoglobulin (IVIG) replacement; Live vaccines are contraindicated.

Question 618: What is the central component of the complement pathway?

A. C3 (Correct Answer)
B. C1
C. C5
D. C2

Explanation: **Explanation:** The complement system is a biochemical cascade of the innate immune system. **C3 is considered the central and most important component** because all three activation pathways—Classical, Alternative, and Lectin—converge at the point of C3 activation. 1. **Why C3 is Correct:** Regardless of how the cascade starts, the critical step is the cleavage of C3 into C3a (anaphylatoxin) and C3b (opsonin) by **C3 convertase**. C3 is the most abundant complement protein in the plasma. Its cleavage leads to the formation of C5 convertase, which initiates the final common lytic pathway. 2. **Why other options are incorrect:** * **C1:** This is the initiator of the **Classical pathway** only (triggered by Antigen-Antibody complexes). It plays no role in the Alternative or Lectin pathways. * **C2:** This is a component involved in the early stages of the Classical and Lectin pathways. It combines with C4b to form C3 convertase (C4b2a). * **C5:** This is the first component of the **Membrane Attack Complex (MAC)**. While vital for cell lysis, it is a downstream effector rather than the central converging point. **High-Yield Clinical Pearls for NEET-PG:** * **C3 deficiency:** The most severe complement deficiency, associated with recurrent pyogenic infections (e.g., *S. pneumoniae*) and Type III hypersensitivity reactions (like SLE). * **C3b function:** Acts as a major **opsonin**, enhancing phagocytosis by binding to CR1 receptors on macrophages. * **C3a & C5a:** Known as **anaphylatoxins**; they trigger mast cell degranulation. C5a is also a potent chemotactic agent for neutrophils. * **Alternative Pathway:** Does not require antibodies; it is activated directly by microbial surfaces (e.g., Endotoxin/LPS).

Question 619: DiGeorge syndrome is characterized by a deficiency of which of the following?

A. B lymphocytes
B. T lymphocytes (Correct Answer)
C. Both B and T lymphocytes
D. Antibodies

Explanation: **Explanation:** **DiGeorge Syndrome (DGS)** is a primary immunodeficiency caused by a microdeletion on chromosome **22q11.2**. The core defect lies in the failure of the **3rd and 4th pharyngeal pouches** to develop during embryogenesis. **Why T lymphocytes is the correct answer:** The thymus gland originates from the 3rd and 4th pharyngeal pouches. In DGS, **thymic hypoplasia or aplasia** occurs, leading to a failure in T-cell maturation. Since the thymus is the primary site where T-cell precursors differentiate and "learn" self-tolerance, its absence results in a profound deficiency of mature **T lymphocytes**, leading to impaired cell-mediated immunity and increased susceptibility to viral, fungal, and protozoal infections. **Why other options are incorrect:** * **A & D (B lymphocytes and Antibodies):** The development of B cells in the bone marrow is initially unaffected. While antibody production (humoral immunity) may be secondary impaired due to a lack of "T-helper" cell signals, the primary and diagnostic deficiency is cellular (T-cell) in nature. * **C (Both B and T lymphocytes):** This pattern is characteristic of **SCID (Severe Combined Immunodeficiency)**, not DiGeorge Syndrome. In DGS, the B-cell count is typically normal. **High-Yield Clinical Pearls for NEET-PG:** * **CATCH-22 Mnemonic:** **C**onotruncal cardiac defects (e.g., Tetralogy of Fallot), **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia (due to parathyroid hypoplasia), and **22**q11 deletion. * **Chest X-ray:** Look for the **absence of a thymic shadow** in a neonate. * **Diagnosis:** Confirmed via **FISH** (Fluorescence In Situ Hybridization) for the 22q11.2 deletion. * **Hypocalcemia:** Occurs because the parathyroid glands also develop from the 3rd/4th pouches; this often presents as neonatal tetany/seizures.

Question 620: Which bacterium is known to produce superantigens?

A. Staphylococcus aureus (Correct Answer)
B. Streptococcus pneumoniae
C. Pseudomonas aeruginosa
D. Clostridium diphtheriae

Explanation: **Explanation:** **Staphylococcus aureus** is the correct answer because it is a classic producer of **Superantigens**. Unlike regular antigens that are processed and presented by MHC II molecules to specific T-cell receptors (TCR), superantigens bypass this processing. They bind directly to the **outer surface of the MHC II molecule** and the **Vβ region of the TCR**. This results in a massive, non-specific activation of T-cells (up to 20% of the body's T-cells), leading to a "cytokine storm" (IL-1, IL-2, TNF-α, and IFN-γ). **Analysis of Options:** * **Staphylococcus aureus (Correct):** Produces **TSST-1** (Toxic Shock Syndrome Toxin-1) and **Staphylococcal Enterotoxins** (causing food poisoning). * **Streptococcus pneumoniae:** Its primary virulence factor is its polysaccharide capsule; it does not produce superantigens. * **Pseudomonas aeruginosa:** Produces **Exotoxin A**, which acts by ADP-ribosylation of Elongation Factor-2 (EF-2), inhibiting protein synthesis. * **Clostridium diphtheriae:** Produces **Diphtheria toxin**, which also inhibits protein synthesis via EF-2 inactivation. **High-Yield Clinical Pearls for NEET-PG:** * **Other Superantigen Producers:** *Streptococcus pyogenes* (SpeA and SpeC toxins causing Streptococcal Toxic Shock-like Syndrome). * **Mechanism:** Superantigens do **not** require processing by Antigen Presenting Cells (APCs). * **Clinical Manifestation:** TSST-1 causes high fever, hypotension, and a diffuse erythematous rash that desquamates (often associated with tampon use or wound infections). * **Food Poisoning:** Staphylococcal enterotoxins are **heat-stable** and cause rapid-onset vomiting (1–6 hours).

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Immunology — MCQs

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