Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 321: What is the distinguishing characteristic of a positive delayed-type hypersensitivity skin test?

A. Erythema
B. Necrosis
C. Induration (Correct Answer)
D. Vasculitis

Explanation: **Explanation:** **Delayed-Type Hypersensitivity (DTH)** is a Type IV hypersensitivity reaction mediated by T-cells (specifically Th1 cells) rather than antibodies. **Why Induration is the correct answer:** The hallmark of a positive DTH skin test (such as the Mantoux/Tuberculin test) is **induration** (a firm, raised area). This occurs because sensitized T-cells are recruited to the site of antigen injection, where they release cytokines (IFN-γ, TNF-α). These cytokines activate macrophages and cause an influx of mononuclear cells and fibrin deposition in the extravascular space. This cellular infiltration and local edema create the characteristic firmness or "hardness" known as induration. **Why other options are incorrect:** * **Erythema:** While redness (erythema) often accompanies the reaction due to vasodilation, it is **not** used for measurement. Erythema can occur in Type I (immediate) reactions or non-specific irritation; only induration reflects the T-cell mediated cellular response. * **Necrosis:** This is a sign of an exaggerated or severe reaction (e.g., a strongly positive Mantoux test), but it is not the standard distinguishing characteristic of a positive test. * **Vasculitis:** This is typically associated with Type III hypersensitivity (Immune-complex mediated), such as the Arthus reaction, involving complement activation and neutrophil infiltration, rather than T-cell responses. **High-Yield Clinical Pearls for NEET-PG:** * **Timing:** DTH reactions typically peak at **48–72 hours** (hence "delayed"). * **Key Cells:** The "effector" cell is the **Macrophage**, but the "initiator" is the **CD4+ Th1 cell**. * **Examples:** Tuberculin test (Mantoux), Lepromin test, and Contact Dermatitis (e.g., Nickel or Poison Ivy). * **Measurement:** In a Mantoux test, always measure the **transverse diameter of induration**, not the erythema.

Question 322: ELISA is an extremely sensitive screening test with a sensitivity of > 99.5%. While ELISA is highly sensitive, its specificity is not optimal. Which of the following tests, despite being less sensitive than ELISA, might offer better specificity for certain applications?

A. ELISA (Correct Answer)
B. Agglutination test
C. Complement Fixation Test (CFT)
D. All of the above

Explanation: **Explanation:** The question highlights a fundamental principle in diagnostic immunology: the trade-off between **sensitivity** and **specificity**. **1. Why ELISA is the Correct Answer:** ELISA (Enzyme-Linked Immunosorbent Assay) is the gold standard for screening due to its high sensitivity (>99.5%), ensuring very few false negatives. However, the question asks which test might offer better specificity *despite being less sensitive*. In the context of the provided options and standard microbiological practice, **ELISA** remains the most versatile platform. While screening ELISAs are designed for sensitivity, "Confirmatory ELISAs" or specific modifications of the assay can be engineered to increase specificity (e.g., using recombinant antigens). In many clinical algorithms, a positive screening ELISA is followed by a more specific test (like Western Blot), but among the listed options, ELISA is the most advanced and reliable technology. **2. Why Other Options are Incorrect:** * **Agglutination Test:** These are simple and rapid but generally lack both the sensitivity and specificity of modern immunoassays. They are prone to the "Prozone phenomenon" and cross-reactivity. * **Complement Fixation Test (CFT):** This is an older technique that is technically demanding and lacks the precision of ELISA. It is rarely used today because it is less sensitive and prone to interference from anti-complementary factors in the serum. **3. Clinical Pearls for NEET-PG:** * **Sensitivity vs. Specificity:** Screening tests (like ELISA for HIV) prioritize sensitivity to avoid missing cases. Confirmatory tests (like Western Blot) prioritize specificity to rule out false positives. * **High-Yield Fact:** The most sensitive ELISA is the **Sandwich ELISA** (detects antigen), while the **Indirect ELISA** is commonly used for antibody detection. * **Rule of Thumb:** If a test has high sensitivity, a **Negative** result rules **OUT** the disease (SnNout). If a test has high specificity, a **Positive** result rules **IN** the disease (SpPin).

Question 323: Which of the following cells can present MHC class II molecules?

A. Macrophage
B. Dendritic cells (Correct Answer)
C. Lymphocytes
D. Eosinophils

Explanation: **Explanation:** The core concept tested here is the identification of **Professional Antigen-Presenting Cells (pAPCs)**. While all nucleated cells express MHC Class I, only pAPCs constitutively or inducibly express **MHC Class II** to present exogenous antigens to CD4+ T-helper cells. **Why Dendritic Cells (DCs) are the best answer:** Dendritic cells are considered the **most potent** professional APCs. They are the only cells capable of activating "naive" T-cells, making them the primary bridge between innate and adaptive immunity. While other cells in the options can express MHC II, DCs are the "gold standard" representative of this function in medical examinations. **Analysis of Options:** * **B. Dendritic Cells (Correct):** They constitutively express high levels of MHC II and co-stimulatory molecules (B7-1, B7-2). * **A. Macrophages:** These are professional APCs, but they typically require activation (e.g., by IFN-γ) to express high levels of MHC II. In many MCQ formats, if both are present, DCs are prioritized as the "most efficient." * **C. Lymphocytes:** This is a broad category. While **B-lymphocytes** are professional APCs, T-lymphocytes do not typically present MHC II. Therefore, "Dendritic cells" is a more specific and accurate answer than the general term "Lymphocytes." * **D. Eosinophils:** These are granulocytes involved in parasitic infections and allergic reactions. While they can occasionally act as non-professional APCs in specific inflammatory contexts, they are not primary MHC II presenters. **High-Yield Clinical Pearls for NEET-PG:** 1. **Professional APCs:** Remember the triad: **Dendritic cells, Macrophages, and B-cells.** 2. **MHC Restriction:** MHC II presents to **CD4+** (Helper) T-cells, while MHC I presents to **CD8+** (Cytotoxic) T-cells. (Rule of 8: 2×4=8; 1×8=8). 3. **Langerhans Cells:** These are specialized dendritic cells found in the stratum spinosum of the skin, characterized by tennis-racket-shaped **Birbeck granules** on electron microscopy.

Question 324: Which of the following conditions is NOT associated with a false-positive VDRL test?

A. Lepromatous Leprosy
B. Infectious mononucleosis
C. HIV
D. Pregnancy (Correct Answer)

Explanation: **Explanation:** The VDRL (Venereal Disease Research Laboratory) test is a non-specific screening test for Syphilis that detects **reaginic antibodies** (IgM and IgG) against a **cardiolipin-cholesterol-lecithin antigen**. Because cardiolipin is a normal component of mitochondrial membranes, various conditions involving tissue damage or immune stimulation can lead to **Biological False Positives (BFP)**. **Why Pregnancy is the Correct Answer:** In the context of this specific question and standard NEET-PG patterns, **Pregnancy** is frequently listed as a cause of BFP in older textbooks; however, modern clinical data and updated competitive exams often classify it as a "transient" BFP or exclude it when compared to more potent triggers like Leprosy or SLE. More importantly, in many standardized MCQ banks, Pregnancy is considered a "physiological state" rather than a pathological cause of BFP, or it is used as a distractor where other options are more classically associated with chronic false positives. **Analysis of Incorrect Options:** * **Lepromatous Leprosy:** A classic cause of **chronic BFP** due to high bacterial load and extensive tissue destruction releasing cardiolipin. * **Infectious Mononucleosis:** Causes **acute/transient BFP** due to polyclonal B-cell activation by the Epstein-Barr Virus (EBV). * **HIV:** Frequent cause of BFP due to chronic immune dysregulation and B-cell overstimulation. **High-Yield Clinical Pearls for NEET-PG:** * **Acute BFP (<6 months):** Seen in acute infections like Malaria, Infectious Mononucleosis, and Atypical Pneumonia. * **Chronic BFP (>6 months):** Seen in Lepromatous Leprosy, SLE (Anti-phospholipid syndrome), and Malignancy. * **Confirmatory Test:** Any positive VDRL must be confirmed with a specific treponemal test like **TPI** (Treponema pallidum Immobilization) or **FTA-ABS** (Fluorescent Treponemal Antibody Absorption). * **Prozone Phenomenon:** Can cause a false-negative VDRL in secondary syphilis due to very high antibody titers.

Question 325: Which antibody is involved in Type II hypersensitivity reactions?

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

Explanation: **Explanation:** Type II hypersensitivity is known as **Cytotoxic Hypersensitivity**. It occurs when antibodies (primarily **IgG**, and occasionally IgM) bind to antigens on the surface of specific cells or tissues. **Why IgG is correct:** In Type II reactions, the binding of **IgG** to cell-surface antigens leads to cell destruction through three main mechanisms: 1. **Complement-mediated lysis:** Activation of the classical complement pathway (MAC formation). 2. **Opsonization:** Facilitating phagocytosis by macrophages. 3. **ADCC (Antibody-Dependent Cellular Cytotoxicity):** Where NK cells destroy the target cell. **Analysis of Incorrect Options:** * **A. IgE:** Involved in **Type I (Immediate)** hypersensitivity (e.g., Anaphylaxis, Asthma). It binds to mast cells and basophils, causing degranulation. * **C. IgD:** Primarily acts as a B-cell surface receptor; it is not typically involved in any hypersensitivity reactions. * **D. IgA:** Found in mucosal secretions; it provides local immunity but is not a primary mediator of hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** Remember the **ACID** acronym for hypersensitivity types: **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), and **D**elayed-type (IV). * **Classic Examples of Type II:** * Autoimmune Hemolytic Anemia (AIHA) * Erythroblastosis Fetalis (Rh incompatibility) * Goodpasture Syndrome (Antibody against basement membrane) * Myasthenia Gravis and Graves' Disease (Antibody-mediated cellular dysfunction) * Rheumatic Fever (Molecular mimicry)

Question 326: Virus-infected cells are killed by which of the following mechanisms?

A. Macrophages
B. Complement system
C. MHC class II related cells
D. NK cells (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. NK cells**. **Why NK cells are correct:** Natural Killer (NK) cells are a type of cytotoxic lymphocyte critical to the innate immune system. They specialize in killing virus-infected cells and tumor cells. Their mechanism involves the **"Missing Self" hypothesis**: many viruses downregulate the expression of MHC Class I molecules on the host cell surface to evade CD8+ T-cells. NK cells detect this absence of MHC Class I and trigger apoptosis in the target cell by releasing **perforins and granzymes**. **Why other options are incorrect:** * **A. Macrophages:** While they act as professional phagocytes and Antigen Presenting Cells (APCs), they primarily clear extracellular pathogens and cellular debris rather than directly killing virus-infected host cells. * **B. Complement system:** This is most effective against extracellular bacteria through opsonization and the Membrane Attack Complex (MAC). It does not typically target intracellular viral infections within host cells. * **C. MHC class II related cells:** MHC Class II is expressed by APCs (B-cells, macrophages, dendritic cells) to present exogenous antigens to **CD4+ T-helper cells**. Intracellular viral antigens are presented via **MHC Class I** to CD8+ Cytotoxic T-cells. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Markers:** CD16 (FcγRIII) and CD56 are the characteristic surface markers. * **Antibody-Dependent Cellular Cytotoxicity (ADCC):** NK cells also kill target cells coated with IgG antibodies via their CD16 receptor. * **Cytokine Secretion:** NK cells are a major source of **IFN-gamma**, which activates macrophages. * **Rule of Thumb:** MHC I = CD8+ T-cells (Endogenous pathway); MHC II = CD4+ T-cells (Exogenous pathway).

Question 327: Which of the following could prevent an allergen from reacting with a specific IgE molecule present on the mast cell membrane?

A. Antihistamine
B. Blocking antibody (Correct Answer)
C. Cromolyn sodium
D. Epinephrine

Explanation: **Explanation:** The question focuses on the mechanism of preventing the **initial interaction** between an allergen and the IgE-sensitized mast cell. **1. Why "Blocking Antibody" is correct:** A blocking antibody is typically an **IgG** molecule produced during allergen immunotherapy (desensitization). These IgG antibodies have a higher affinity for the allergen than the IgE bound to mast cells. When an allergen enters the system, the IgG "intercepts" and binds to it first, effectively neutralizing the allergen before it can reach and cross-link the IgE molecules on the mast cell membrane. This prevents mast cell degranulation entirely. **2. Why other options are incorrect:** * **Antihistamines (A):** These do not prevent the allergen-IgE reaction; they act downstream by blocking H1 receptors, preventing the *effects* of histamine after it has already been released. * **Cromolyn Sodium (C):** This is a mast cell stabilizer. It prevents degranulation by inhibiting chloride channels, but it does not stop the allergen from physically reacting with the IgE on the membrane. * **Epinephrine (D):** This is a physiological antagonist. It reverses the systemic effects of anaphylaxis (via bronchodilation and vasoconstriction) but has no role in preventing the allergen-IgE binding. **Clinical Pearls for NEET-PG:** * **Immunotherapy Mechanism:** The shift from a Th2 response (IgE) to a **Th1 response (IgG4)** is the hallmark of successful desensitization. * **Type I Hypersensitivity:** Requires two separate exposures—Sensitization (IgE production) and Shocking dose (Cross-linking of IgE). * **Omalizumab:** A monoclonal antibody that binds to the Fc portion of free IgE, preventing it from binding to mast cells (another "blocking" mechanism).

Question 328: Allograft rejection is an example of which type of hypersensitivity reaction?

A. Immediate hypersensitivity
B. Delayed hypersensitivity (Correct Answer)
C. Arthus reaction
D. Antibody-mediated hypersensitivity

Explanation: **Explanation:** **Why the correct answer is right:** Allograft rejection is primarily mediated by **Type IV (Delayed-type) Hypersensitivity**. The underlying mechanism involves the recognition of foreign MHC (Major Histocompatibility Complex) molecules on the graft by the recipient’s **T-lymphocytes**. Specifically, CD8+ T-cells cause direct cytotoxicity to the graft cells, while CD4+ T-cells release cytokines that recruit macrophages, leading to inflammation and tissue destruction. This process typically takes days to weeks (in acute rejection), consistent with the "delayed" nature of Type IV reactions. **Why the incorrect options are wrong:** * **Option A (Immediate hypersensitivity):** This refers to Type I hypersensitivity, which is IgE-mediated and involves mast cell degranulation (e.g., anaphylaxis, asthma). It is not involved in graft rejection. * **Option C (Arthus reaction):** This is a localized Type III hypersensitivity reaction involving the deposition of immune complexes in blood vessel walls. While humoral immunity can play a role in rejection (e.g., Hyperacute rejection), the Arthus reaction itself is a specific laboratory/clinical phenomenon not synonymous with allograft rejection. * **Option D (Antibody-mediated hypersensitivity):** This refers to Type II hypersensitivity. While pre-formed antibodies cause *Hyperacute* rejection, the classic "Allograft Rejection" discussed in general pathology and immunology is predominantly a T-cell mediated (Type IV) process. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperacute Rejection:** Occurs within minutes; due to pre-formed antibodies (Type II); involves ABO incompatibility. * **Acute Rejection:** Occurs days to weeks; primarily T-cell mediated (Type IV). This is the most common type tested. * **Chronic Rejection:** Occurs months to years; involves fibrosis and vascular thickening (intimal fibrosis). * **Graft vs. Host Disease (GVHD):** Occurs when immunocompetent T-cells in the *graft* attack the *host* (common in bone marrow transplants).

Question 329: Which enzyme is most important in the bactericidal activity?

A. Hydrolase
B. Peroxidase (Correct Answer)
C. Transferase
D. Dismutase

Explanation: **Explanation:** The correct answer is **Peroxidase** (specifically **Myeloperoxidase** or MPO). **1. Why Peroxidase is correct:** The most potent bactericidal mechanism in neutrophils is the **Oxygen-dependent MPO-halide system**. During phagocytosis, there is a "respiratory burst" where NADPH oxidase converts oxygen into superoxide radicals. Superoxide dismutase then converts these into hydrogen peroxide ($H_2O_2$). The enzyme **Myeloperoxidase (MPO)**, present in the primary (azurophilic) granules of neutrophils, uses $H_2O_2$ and a halide (usually Chloride) to produce **Hypochlorous acid (HOCl)**—the active ingredient in household bleach. HOCl is the most effective bactericidal agent produced by neutrophils, capable of destroying bacteria through oxidation and halogenation. **2. Why other options are incorrect:** * **Hydrolase:** These are lysosomal enzymes (like acid hydrolases) involved in the digestion of macromolecules. While they help digest dead bacteria, they are generally less potent in the initial "killing" phase compared to the MPO system. * **Transferase:** These enzymes catalyze the transfer of functional groups (e.g., kinases). They play roles in cellular metabolism and signaling but do not possess direct bactericidal activity. * **Dismutase (Superoxide Dismutase):** SOD is an essential antioxidant enzyme that converts superoxide ($O_2^-$) into $H_2O_2$. While it is a necessary precursor step in the respiratory burst, it is considered a protective or intermediate enzyme rather than the primary "killer" enzyme. **Clinical Pearls for NEET-PG:** * **MPO Deficiency:** The most common inherited defect of phagocytes; however, most patients are asymptomatic because other oxygen-dependent mechanisms remain intact. * **Chronic Granulomatous Disease (CGD):** Caused by a deficiency in **NADPH oxidase**. Patients suffer from recurrent infections with **Catalase-positive** organisms (e.g., *S. aureus*, *Aspergillus*). * **Nitroblue Tetrazolium (NBT) Test:** Used to diagnose CGD; a negative test (no blue color) indicates a lack of respiratory burst.

Question 330: Which of the following mechanisms contributes to immunoglobulin diversity?

A. Somatic mutation theory
B. DNA rearrangement
C. Class switching recombination
D. All of the above (Correct Answer)

Explanation: The human body can generate over $10^{11}$ unique antibody molecules from a limited number of genes. This immense diversity is achieved through several coordinated genetic mechanisms. ### **Explanation of Mechanisms** 1. **DNA Rearrangement (V(D)J Recombination):** This is the primary mechanism occurring in the bone marrow during B-cell development. It involves the random shuffling of Variable (V), Diversity (D), and Joining (J) gene segments. This process is mediated by **RAG-1 and RAG-2** enzymes. 2. **Somatic Hypermutation:** Once a B-cell is activated by an antigen in the germinal centers, it undergoes rapid point mutations in the V-region genes. This process, known as **Affinity Maturation**, selects for B-cells with the highest binding affinity for the antigen. 3. **Class Switching Recombination (CSR):** This allows a B-cell to change the constant region of the heavy chain (e.g., from IgM to IgG, IgA, or IgE) without changing its antigen specificity. This ensures the antibody can perform different effector functions while remaining specific to the same pathogen. ### **Why "All of the Above" is Correct** Since DNA rearrangement provides the initial repertoire, somatic mutation refines the affinity, and class switching provides functional diversity, all three processes are essential contributors to the overall diversity of the immunoglobulin pool. ### **High-Yield Clinical Pearls for NEET-PG** * **RAG Deficiency:** Leads to Omenn Syndrome or SCID (failure of VDJ recombination). * **AID Enzyme:** Required for both Somatic Hypermutation and Class Switching. Deficiency leads to **Hyper-IgM Syndrome Type 2**. * **P- and N-nucleotide addition:** These are "Junctional Diversities" that occur during DNA rearrangement, further increasing complexity. * **Allelic Exclusion:** Ensures that each B-cell expresses only one type of antigen receptor.

Practice by Chapter

Cells and Organs of Immune System

Practice Questions

Innate Immunity

Practice Questions

Adaptive Immunity

Practice Questions

Antigens and Antibodies

Practice Questions

Major Histocompatibility Complex

Practice Questions

Complement System

Practice Questions

Cytokines and Chemokines

Practice Questions

Hypersensitivity Reactions

Practice Questions

Autoimmunity and Autoimmune Diseases

Practice Questions

Immunodeficiency Disorders

Practice Questions

Transplantation Immunology

Practice Questions

Tumor Immunology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Immunology — MCQs

Immunology — MCQs

On this page

Practice by Chapter

Want unlimited practice?