Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 791: Immunoglobulin is not used in the prophylaxis of which of the following conditions?

A. Hepatitis A
B. Varicella
C. Influenza (Correct Answer)
D. Measles

Explanation: **Explanation:** The correct answer is **Influenza**. Immunoglobulins (passive immunization) are used to provide immediate, short-term protection against specific infections, particularly after exposure. However, for **Influenza**, prophylaxis is achieved through **active immunization (vaccines)** or **antiviral chemoprophylaxis** (e.g., Oseltamivir). Immunoglobulin therapy is not a standard clinical practice for Influenza because the virus undergoes frequent antigenic drift and shift, and the primary defense mechanism required is local mucosal immunity (IgA) and T-cell response, which systemic IgG administration does not effectively provide. **Analysis of Options:** * **Hepatitis A:** Normal Human Immunoglobulin (NHIG) is used for pre-exposure and post-exposure prophylaxis (within 2 weeks) in non-immune individuals traveling to endemic areas or following close contact. * **Varicella:** Varicella-Zoster Immunoglobulin (VZIG) is indicated for post-exposure prophylaxis in high-risk individuals (e.g., immunocompromised, pregnant women, or neonates) to prevent or modify the disease. * **Measles:** NHIG can prevent or modify measles if given within 6 days of exposure, especially in infants under 9 months or immunocompromised contacts. **NEET-PG High-Yield Pearls:** * **Passive-Active Immunization:** For Rabies, Hepatitis B, and Tetanus, both immunoglobulin and vaccine are given simultaneously at different sites. * **NHIG vs. Specific IG:** NHIG is used for Hepatitis A and Measles. Specific (Hyperimmune) IGs are used for Hepatitis B (HBIG), Rabies (RIG), Tetanus (TIG), and Varicella (VZIG). * **Contraindication:** Live vaccines (like MMR or Varicella) should generally be delayed for 3–11 months after receiving immunoglobulin therapy to prevent interference with the immune response.

Question 792: A deficiency of which of the following cells can predispose to candidiasis?

A. Eosinophils
B. Macrophages
C. Plasma cells
D. T Lymphocytes (Correct Answer)

Explanation: **Explanation:** The correct answer is **T Lymphocytes**. The body’s defense against *Candida albicans* is a dual mechanism involving both innate and adaptive immunity. 1. **Why T Lymphocytes are correct:** Cell-Mediated Immunity (CMI), specifically **Th17 and Th1 cells**, is crucial for controlling mucocutaneous fungal infections. T lymphocytes produce cytokines (like IL-17 and IL-22) that recruit neutrophils and maintain mucosal integrity. A deficiency in T-cells (as seen in HIV/AIDS or Chronic Mucocutaneous Candidiasis) leads to persistent **mucocutaneous candidiasis** (oral thrush, esophagitis). 2. **Why other options are incorrect:** * **Eosinophils:** These are primarily involved in defense against helminthic (parasitic) infections and type I hypersensitivity reactions; they play a negligible role in fungal defense. * **Macrophages:** While they act as antigen-presenting cells and can ingest yeast, they are not the primary cell type whose *deficiency* characteristically predisposes to candidiasis compared to T-cells or neutrophils. * **Plasma cells:** These produce antibodies (Humoral Immunity). While antibodies can prevent systemic spread, they are not the primary defense against the localized mucosal colonization of *Candida*. **Clinical Pearls for NEET-PG:** * **Dual Defense Rule:** * **T-cell deficiency** predisposes to **Mucocutaneous Candidiasis** (e.g., HIV patients). * **Neutrophil deficiency** (Neutropenia) predisposes to **Disseminated/Systemic Candidiasis** (e.g., chemotherapy patients). * **Th17 cells** are the specific subset of T-cells most vital for fungal immunity at mucosal surfaces. * **Chronic Mucocutaneous Candidiasis (CMC)** is often associated with AIRE gene mutations or STAT1 signaling defects.

Question 793: Which of the following events occurs first in the differentiation sequence of human B cells in the bone marrow?

A. Cytoplasmic mu chains present in the B cell
B. Immunoglobulin heavy chain rearrangement (Correct Answer)
C. Immunoglobulin light chain rearrangement
D. Surface IgD and IgM present on the B cell

Explanation: ### Explanation The differentiation of B cells in the bone marrow follows a highly regulated, sequential genetic program. The primary goal of this process is the successful assembly of a functional B-cell receptor (BCR). **1. Why Option B is Correct:** The very first step in B-cell commitment is the **rearrangement of the Immunoglobulin (Ig) heavy chain genes**. This occurs during the **Pro-B cell stage**. The process involves VDJ recombination (joining of Variable, Diversity, and Joining gene segments). Only after a functional heavy chain is produced can the cell proceed to subsequent stages. **2. Analysis of Incorrect Options:** * **Option A (Cytoplasmic mu chains):** This occurs during the **Pre-B cell stage**. It is the result of successful heavy chain rearrangement. Therefore, it is a downstream event of Option B. * **Option C (Light chain rearrangement):** This occurs **after** the heavy chain is successfully formed and expressed. Light chain rearrangement (VJ joining) happens during the late Pre-B cell stage. * **Option D (Surface IgD and IgM):** This characterizes the **Mature B cell**. Immature B cells express only surface IgM; the co-expression of IgM and IgD signifies that the B cell is ready to leave the bone marrow and enter the peripheral lymphoid organs. **3. NEET-PG High-Yield Pearls:** * **Sequence of Stages:** Pro-B $\rightarrow$ Pre-B $\rightarrow$ Immature B $\rightarrow$ Mature B. * **Allelic Exclusion:** Once one heavy chain allele rearranges successfully, the other is "shut off" to ensure each B cell has a single specificity. * **Surrogate Light Chain:** In the Pre-B stage, the $\mu$ heavy chain associates with a "surrogate" light chain to test its functionality before actual light chain rearrangement begins. * **Bruton’s Agammaglobulinemia:** A classic clinical correlation where B-cell development is arrested at the **Pre-B cell stage** due to a mutation in the B-cell tyrosine kinase (BTK) gene.

Question 794: What is the most important Human Leukocyte Antigen (HLA) for organ transplantation and tissue typing?

A. HLA-A
B. HLA-B
C. HLA-C
D. HLA-D (Correct Answer)

Explanation: **Explanation:** The Major Histocompatibility Complex (MHC) in humans, known as the **Human Leukocyte Antigen (HLA)** system, is divided into Class I (A, B, C) and Class II (DR, DQ, DP). **Why HLA-D is the Correct Answer:** HLA-D (specifically the **HLA-DR** locus) is considered the most critical for organ transplantation and tissue typing. This is because Class II antigens are primarily responsible for initiating the **Mixed Lymphocyte Reaction (MLR)** and the proliferation of T-helper cells. In clinical transplantation, a mismatch at the HLA-D/DR locus is the strongest predictor of acute graft rejection and Graft-versus-Host Disease (GVHD). Therefore, matching at the D-locus is prioritized over Class I matching to ensure long-term graft survival. **Analysis of Incorrect Options:** * **HLA-A & HLA-B:** These are Class I MHC molecules. While they are important for tissue typing and are routinely matched (especially in kidney transplants), they are generally considered less immunogenic than HLA-DR in the context of initiating the primary immune response against a graft. * **HLA-C:** This is also a Class I molecule, but it has the lowest level of polymorphism and clinical significance among the major HLA loci in routine transplantation. **NEET-PG High-Yield Pearls:** * **MHC Class I (A, B, C):** Present endogenous antigens to **CD8+** T-cells. * **MHC Class II (DR, DQ, DP):** Present exogenous antigens to **CD4+** T-cells. * **Best Match:** Identical twins provide a perfect HLA match. Among siblings, there is a **25% (1 in 4)** chance of a complete HLA match. * **Ankylosing Spondylitis:** Strongly associated with **HLA-B27**. * **Narcolepsy:** Strongly associated with **HLA-DR2/DQB1**.

Question 795: Paul Bunnell antibodies are reactive in all except?

A. Ox red blood cells (Correct Answer)
B. Sheep red blood cells
C. Dog red blood cells
D. Horse red blood cells

Explanation: The **Paul-Bunnell test** is a classic diagnostic tool used to detect **Infectious Mononucleosis (IM)** caused by the Epstein-Barr virus (EBV). The test identifies **heterophile antibodies**, which are IgM antibodies produced during IM that have the unique property of agglutinating red blood cells (RBCs) from different animal species. ### Why "Ox red blood cells" is the correct answer: Paul-Bunnell antibodies are defined by their ability to agglutinate **Sheep, Horse, and Dog RBCs**. However, they are **specifically absorbed by Ox (Beef) RBCs**. In the laboratory, if the patient's serum is pre-treated with Ox RBCs, the Paul-Bunnell antibodies are removed, and agglutination will no longer occur. Therefore, they are considered **reactive against** sheep/horse/dog cells but are **neutralized/absorbed by** ox cells. ### Analysis of Options: * **B, C, and D (Sheep, Dog, Horse RBCs):** These are the target antigens. Paul-Bunnell antibodies show positive agglutination reactions with these cells. Horse RBCs are currently the preferred substrate for the rapid "Monospot" test due to higher sensitivity. ### High-Yield Clinical Pearls for NEET-PG: 1. **Heterophile Antibodies:** These are "multispecific" antibodies that react with antigens across species boundaries but are **not** specific to EBV viral antigens. 2. **Differential Absorption (Davidsohn Differential Test):** * **IM Antibodies:** Absorbed by **Ox RBCs**; NOT absorbed by **Guinea pig kidney cells**. * **Forssman Antibodies:** Absorbed by **Guinea pig kidney cells**; NOT absorbed by Ox RBCs. * **Serum Sickness Antibodies:** Absorbed by **BOTH** Ox RBCs and Guinea pig kidney cells. 3. **Age Factor:** The Paul-Bunnell test is often **negative** in children under 5 years old with EBV infection.

Question 796: Which of the following cells expresses the CD3 receptor?

A. T cells (Correct Answer)
B. B cells
C. Macrophages
D. Eosinophils

Explanation: **Explanation:** **CD3 (Cluster of Differentiation 3)** is a definitive lineage marker for **T cells**. It is a protein complex composed of four distinct chains (gamma, delta, and two epsilon chains) that associate non-covalently with the **T-cell receptor (TCR)**. Its primary physiological role is signal transduction; while the TCR recognizes the antigen-MHC complex, the CD3 complex transmits the activation signal into the cytoplasmic compartment of the T cell. Because CD3 is required for the surface expression of the TCR, it is present on all mature T lymphocytes (both Helper T cells/CD4+ and Cytotoxic T cells/CD8+). **Analysis of Incorrect Options:** * **B cells:** These are characterized by markers such as **CD19, CD20, and CD21**. They express Surface Immunoglobulins (sIg) rather than TCR/CD3 complexes. * **Macrophages:** These are myeloid lineage cells. Their characteristic markers include **CD14** (receptor for LPS) and **CD16/CD64**. * **Eosinophils:** These are granulocytes identified by their bilobed nuclei and eosinophilic granules. They do not express lymphoid markers like CD3. **High-Yield Clinical Pearls for NEET-PG:** * **Pan-T cell marker:** CD3 is considered the most reliable "Pan-T cell marker" in immunohistochemistry to identify T-cell lymphomas. * **Muromonab-CD3 (OKT3):** A monoclonal antibody directed against CD3 used as an immunosuppressant to prevent acute organ transplant rejection. * **Double Negative/Positive:** During thymic T-cell maturation, cells start as CD4-/CD8- (Double Negative), then become CD4+/CD8+ (Double Positive) before maturing into single-positive T cells; however, **CD3 expression** increases as they mature.

Question 797: Which of the following is a function of Interleukin-1 (IL-1)?

A. T lymphocyte activation (Correct Answer)
B. Delayed wound healing
C. Increased pain perception
D. Decreased PMN release from bone marrow

Explanation: **Explanation:** Interleukin-1 (IL-1) is a key pro-inflammatory cytokine primarily produced by activated macrophages and monocytes. It plays a central role in the "dual-signal" model of immune activation. **1. Why Option A is Correct:** IL-1 acts as a potent co-stimulator for **T lymphocyte activation**. When an Antigen-Presenting Cell (APC) presents an antigen to a T-cell via the MHC-TCR complex, it also releases IL-1. This cytokine induces T-cells to produce **Interleukin-2 (IL-2)** and express IL-2 receptors, leading to T-cell proliferation and the transition from the G0 to G1 phase of the cell cycle. **2. Why the Other Options are Incorrect:** * **Option B:** IL-1 actually **promotes wound healing** by stimulating the proliferation of fibroblasts and the synthesis of collagen. * **Option C:** While IL-1 is involved in the inflammatory cascade, it does not directly increase pain perception in the same way prostaglandins or bradykinin do; its primary systemic effects are fever and acute-phase reactant synthesis. * **Option D:** IL-1 causes **increased release of PMNs (neutrophils)** from the bone marrow, often leading to a "left shift" (neutrophilia with immature forms) during acute infection. **High-Yield Clinical Pearls for NEET-PG:** * **Endogenous Pyrogen:** IL-1 is the primary mediator of fever. It acts on the anterior hypothalamus to increase prostaglandin E2 (PGE2) production, raising the thermoregulatory set-point. * **Acute Phase Response:** Along with IL-6 and TNF-α, IL-1 stimulates the liver to produce acute-phase proteins (e.g., CRP, Fibrinogen). * **Osteoclast Activation:** In the context of bone, IL-1 is also known as **Osteoclast Activating Factor (OAF)**, leading to bone resorption. * **Anakinra:** This is a recombinant IL-1 receptor antagonist used clinically in Rheumatoid Arthritis.

Question 798: T cells mature in:

A. Thyroid
B. Tongue
C. Thymus (Correct Answer)
D. Trachea

Explanation: **Explanation:** The correct answer is **Thymus (Option C)**. **1. Why Thymus is correct:** T lymphocytes (T cells) originate from hematopoietic stem cells in the **bone marrow** but must migrate to the **thymus** to undergo maturation and differentiation. In the thymus, immature T cells (thymocytes) undergo two critical selection processes: * **Positive Selection:** Ensures T cells can recognize the body's MHC molecules. * **Negative Selection:** Eliminates self-reactive T cells to prevent autoimmunity. Once matured, they express either CD4 or CD8 markers and migrate to secondary lymphoid organs. **2. Why other options are incorrect:** * **Thyroid (A):** An endocrine gland responsible for metabolism via T3 and T4 hormones; it has no role in lymphocyte maturation. * **Tongue (B):** A muscular organ involved in gustation and deglutition. * **Trachea (D):** A cartilaginous tube serving as the primary airway for the respiratory system. **3. NEET-PG High-Yield Pearls:** * **Primary Lymphoid Organs:** Bone marrow (B-cell maturation) and Thymus (T-cell maturation). * **DiGeorge Syndrome:** A classic exam topic where thymic hypoplasia leads to T-cell deficiency and recurrent viral/fungal infections. * **Hassall’s Corpuscles:** These are characteristic histological features found in the medulla of the thymus. * **Involution:** The thymus is most active during childhood and undergoes fatty replacement (involution) after puberty, though T-cell production continues at a lower rate.

Question 799: Which of the following is an example of Type-II hypersensitivity?

A. Contact dermatitis
B. Hemolytic anemia
C. Serum sickness (Correct Answer)
D. Good pasture syndrome

Explanation: **Explanation:** The question asks for an example of **Type II hypersensitivity**, but there is a discrepancy in the provided key: **Serum sickness is actually a classic example of Type III hypersensitivity.** In Type III reactions, soluble antigen-antibody complexes circulate and deposit in tissues (like joints and kidneys), activating complement and causing systemic inflammation. **Why the options are classified as follows:** * **B. Hemolytic Anemia & D. Goodpasture Syndrome:** Both are classic **Type II (Cytotoxic) hypersensitivity** reactions. In Type II, antibodies (IgG/IgM) bind to antigens on specific cell surfaces or extracellular matrix, leading to cell destruction via complement activation or ADCC. * *Hemolytic Anemia:* Antibodies target RBC surfaces. * *Goodpasture Syndrome:* Antibodies target the glomerular basement membrane (anti-GBM). * **C. Serum Sickness (Marked Correct):** This is **Type III**. It occurs when foreign proteins (antigens) are injected, leading to widespread immune-complex deposition. * **A. Contact Dermatitis:** This is **Type IV (Delayed-type)** hypersensitivity, mediated by T-cells rather than antibodies. **Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity (ACID):** * **A**naphylactic (Type I): IgE-mediated (Asthma, Urticaria). * **C**ytotoxic (Type II): Antibody against cell surface (Myasthenia Gravis, Rheumatic Fever). * **I**mmune-Complex (Type III): Soluble complexes (SLE, Post-streptococcal GN, Arthus reaction). * **D**elayed (Type IV): T-cell mediated (Mantoux test, Graft rejection). * **High-Yield Note:** If this question appeared in an exam with "Serum Sickness" as the key, it is likely a technical error in the question bank, as both B and D are technically correct examples of Type II.

Question 800: Which of the following is an example of a heterophile antigen?

A. Forssman antigen (Correct Answer)
B. Cryptococcus polysaccharide
C. Protein A of Staphylococcus
D. All of the above

Explanation: ### Explanation **Concept of Heterophile Antigens** Heterophile antigens are closely related antigens present in two or more completely different species (e.g., humans, animals, plants, or bacteria). If an individual produces antibodies against one, those antibodies will cross-react with the heterophile antigen of the other species. This principle is frequently used in diagnostic serology. **Why Option A is Correct:** The **Forssman antigen** is the classic example of a heterophile antigen. It is a lipid-carbohydrate complex found in the red blood cells of many species (like sheep, horses, and guinea pigs) and some bacteria, but it is notably absent in rabbits. It is clinically significant because it can induce the production of "Forssman antibodies," which are distinguished from infectious mononucleosis antibodies in the differential diagnosis of febrile illnesses. **Why Other Options are Incorrect:** * **B. Cryptococcus polysaccharide:** This is a specific capsular antigen (Glucuronoxylomannan) used for the diagnosis of Cryptococcosis via the Latex Agglutination Test. It is specific to the fungus and does not exhibit heterophile cross-reactivity across unrelated species. * **C. Protein A of Staphylococcus:** This is a surface protein found in *Staphylococcus aureus* that binds to the Fc portion of IgG. While it is an important virulence factor used in co-agglutination tests, it is a specific bacterial protein, not a heterophile antigen. **High-Yield Clinical Pearls for NEET-PG:** * **Paul-Bunnell Test:** Uses heterophile antibodies produced during **Infectious Mononucleosis** (EBV) that cross-react with and agglutinate sheep RBCs. * **Weil-Felix Reaction:** A classic heterophile antibody test where antibodies produced against *Rickettsia* cross-react with **Proteus** antigens (OX-19, OX-2, OX-K). * **Cold Agglutinins:** Seen in *Mycoplasma pneumoniae* infections, where antibodies cross-react with human RBC 'I' antigens at low temperatures.

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Immunology — MCQs

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