Immunology Practice Questions

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

Induration. **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.

Q: Which antibody is involved in Type II hypersensitivity reactions?

IgG. **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)

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

NK cells. **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).

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

Blocking antibody. **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).

Q: Which of the following mechanisms contributes to immunoglobulin diversity?

All of the above. 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.

Question 1

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

Accepted Answer

Induration

Answer

Erythema

Answer

Necrosis

Answer

Vasculitis

Question 2

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?

Accepted Answer

ELISA

Answer

Agglutination test

Answer

Complement Fixation Test (CFT)

Answer

All of the above

Question 3

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

Accepted Answer

Dendritic cells

Answer

Macrophage

Answer

Lymphocytes

Answer

Eosinophils

Question 4

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

Accepted Answer

Pregnancy

Answer

Lepromatous Leprosy

Answer

Infectious mononucleosis

Answer

HIV

Question 5

Which antibody is involved in Type II hypersensitivity reactions?

Accepted Answer

IgG

Answer

IgE

Answer

IgD

Answer

IgA

Question 6

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

Accepted Answer

NK cells

Answer

Macrophages

Answer

Complement system

Answer

MHC class II related cells

Question 7

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

Accepted Answer

Blocking antibody

Answer

Antihistamine

Answer

Cromolyn sodium

Answer

Epinephrine

Question 8

Allograft rejection is an example of which type of hypersensitivity reaction?

Accepted Answer

Delayed hypersensitivity

Answer

Immediate hypersensitivity

Answer

Arthus reaction

Answer

Antibody-mediated hypersensitivity

Question 9

Which enzyme is most important in the bactericidal activity?

Accepted Answer

Peroxidase

Answer

Hydrolase

Answer

Transferase

Answer

Dismutase

Question 10

Which of the following mechanisms contributes to immunoglobulin diversity?

Accepted Answer

All of the above

Answer

Somatic mutation theory

Answer

DNA rearrangement

Answer

Class switching recombination

Immunology — MCQs

Immunology — MCQs

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