Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 301: Which type of hypersensitivity reaction is mediated by cell-mediated immunity?

A. Type I
B. Type II
C. Type III
D. Type IV (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Type IV** **Underlying Concept:** Type IV hypersensitivity is the only type that is **cell-mediated** rather than antibody-mediated. It is also known as **Delayed-Type Hypersensitivity (DTH)** because it typically takes 48–72 hours to manifest. The reaction is mediated by sensitized **T-lymphocytes** (CD4+ Th1 cells or CD8+ cytotoxic T cells). When exposed to an antigen, these cells release cytokines (like IFN-γ) that recruit and activate macrophages, leading to tissue inflammation and damage. **Why the other options are incorrect:** * **Type I (Immediate):** Mediated by **IgE antibodies** binding to mast cells and basophils, leading to histamine release (e.g., Anaphylaxis, Asthma). * **Type II (Cytotoxic):** Mediated by **IgG or IgM antibodies** directed against antigens on specific cell surfaces or tissues (e.g., Rh incompatibility, Myasthenia Gravis). * **Type III (Immune-Complex):** Mediated by the deposition of **antigen-antibody complexes** in tissues, which activates the complement system (e.g., SLE, Post-streptococcal glomerulonephritis). **High-Yield Clinical Pearls for NEET-PG:** * **Classic Examples of Type IV:** Mantoux (Tuberculin) test, Contact Dermatitis (poison ivy, nickel), Graft vs. Host Disease (GVHD), and Granuloma formation (Leprosy, Sarcoidosis). * **Mnemonic (ACID):** * **A** - **A**naphylactic (Type I) * **C** - **C**ytotoxic (Type II) * **I** - **I**mmune Complex (Type III) * **D** - **D**elayed/Cell-mediated (Type IV) * **Key Cells:** Type IV is the only one involving **T-cells** and **Macrophages**; Types I, II, and III all require **B-cells** (to produce antibodies).

Question 302: Which cells recognize MHC Class I molecules?

A. CD4 T cells
B. CD8 T cells (Correct Answer)
C. Dendritic cells
D. Macrophages

Explanation: **Explanation:** The recognition of Major Histocompatibility Complex (MHC) molecules is governed by the **MHC Restriction Rule**, which ensures that the immune system responds appropriately to different types of antigens. **Why CD8 T cells are correct:** CD8+ T cells (Cytotoxic T lymphocytes) specifically recognize antigens presented on **MHC Class I** molecules. This interaction is stabilized by the CD8 co-receptor, which binds to the α3 domain of the MHC I heavy chain. Since MHC Class I is expressed on almost all nucleated cells, this allows CD8 T cells to monitor and destroy any cell infected by viruses or transformed by cancer (endogenous antigens). **Why other options are incorrect:** * **CD4 T cells:** These cells recognize antigens presented on **MHC Class II** molecules. The CD4 co-receptor binds to the β2 domain of MHC II. This interaction is essential for "helper" functions, such as activating B cells and macrophages. * **Dendritic cells & Macrophages:** These are **Professional Antigen-Presenting Cells (APCs)**. While they *express* both MHC I and MHC II to present antigens to T cells, they are not the cells that "recognize" the MHC molecule in the context of initiating an effector response; rather, they are the presenters. **High-Yield NEET-PG Pearls:** 1. **The Rule of 8:** A simple mnemonic to remember MHC restriction: * 4 (CD4) × 2 (MHC II) = **8** * 8 (CD8) × 1 (MHC I) = **8** 2. **Structure:** MHC I consists of a heavy chain and a **β2-microglobulin**; MHC II consists of α and β chains. 3. **Cross-presentation:** Dendritic cells have the unique ability to present exogenous antigens on MHC I to activate CD8 T cells (priming).

Question 303: Graves disease is an example of which of the following immunologic processes?

A. Autoimmune disease associated with HLA gene B27
B. Autoimmune disease associated with HLA gene DR3 (Correct Answer)
C. Immune deficiency associated with HLA gene DR2
D. Immune deficiency associated with HLA gene DR4

Explanation: **Explanation:** **Graves’ Disease** is an organ-specific autoimmune disorder characterized by hyperthyroidism due to the production of **Thyroid Stimulating Immunoglobulins (TSI)**. These are Type II Hypersensitivity antibodies that bind to and activate the TSH receptor, mimicking the action of TSH. 1. **Why Option B is Correct:** Susceptibility to Graves’ disease is strongly linked to the **HLA-DR3** gene (and HLA-B8). The Human Leukocyte Antigen (HLA) system plays a crucial role in antigen presentation; specific alleles like DR3 are thought to inefficiently clear self-reactive T-cells or present thyroid-derived peptides in a way that triggers an autoimmune response. 2. **Analysis of Incorrect Options:** * **Option A (HLA-B27):** This is classically associated with **Seronegative Spondyloarthropathies**, remembered by the mnemonic **PAIR**: **P**soriatic arthritis, **A**nkylosing spondylitis (strongest association), **I**nflammatory bowel disease, and **R**eactive arthritis. * **Option C (HLA-DR2):** This allele is associated with Multiple Sclerosis, Hay fever, Goodpasture syndrome, and SLE (along with DR3). It is not primarily linked to Graves'. * **Option D (HLA-DR4):** This is the high-yield association for **Rheumatoid Arthritis** ("Four-thritis") and Type 1 Diabetes Mellitus (which is also linked to DR3). **High-Yield Clinical Pearls for NEET-PG:** * **HLA-DR3 Associations:** Graves’ disease, SLE, Myasthenia Gravis, and Type 1 Diabetes Mellitus. * **HLA-DR4 Associations:** Rheumatoid Arthritis, Pemphigus Vulgaris, and Type 1 Diabetes Mellitus. * **Graves’ Triad:** Hyperthyroidism (Goiter), Exophthalmos (Proptosis), and Pretibial Myxedema. * **Pathogenesis:** It is a **Type II (Cytotoxic) Hypersensitivity** reaction, specifically the "Stimulatory" subtype.

Question 304: Which immunoglobulin is the primary mediator of Type I hypersensitivity reactions?

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

Explanation: **Explanation:** **Type I Hypersensitivity (Immediate)** is an allergic reaction triggered by the interaction of an allergen with specific antibodies. **Why IgE is the correct answer:** IgE is the primary mediator of Type I hypersensitivity. Upon first exposure to an allergen, B-cells undergo class switching to produce IgE, which binds to high-affinity **FcεRI receptors** on the surface of **mast cells and basophils** (Sensitization). Upon re-exposure, the allergen cross-links these bound IgE molecules, triggering degranulation and the release of vasoactive amines like **histamine**, leading to clinical manifestations like anaphylaxis, asthma, or urticaria. **Why other options are incorrect:** * **IgD:** Primarily acts as a B-cell surface receptor; its exact systemic function is less defined and it plays no role in hypersensitivity. * **IgM:** The first antibody produced in a primary immune response; it is involved in **Type II** (cytotoxic) and **Type III** (immune-complex) reactions via complement activation. * **IgG:** The most abundant serum antibody. While it mediates **Type II and Type III** hypersensitivity, it actually acts as a "blocking antibody" in Type I (the basis for desensitization therapy). **High-Yield Clinical Pearls for NEET-PG:** * **Coombs and Gell Classification:** Type I is "Immediate," Type II is "Cytotoxic," Type III is "Immune-Complex mediated," and Type IV is "Delayed/Cell-mediated." * **Key Cells:** Mast cells are the central effector cells in Type I reactions. * **Eosinophilia:** Often associated with Type I reactions due to IL-5 stimulation. * **Prausnitz-Küstner (PK) reaction:** A classic (though now historical) test used to demonstrate IgE-mediated passive transfer of allergy.

Question 305: The binding site for complement on the IgG molecule is located in which domain?

A. VL domain
B. CL domain
C. CH1 domain
D. CH2 domain (Correct Answer)

Explanation: ### Explanation The correct answer is **D. CH2 domain**. **1. Why the CH2 domain is correct:** The classical complement pathway is initiated when the **C1q** component of the C1 complex binds to the Fc portion of an antibody. For **IgG**, the specific binding site for C1q is located in the **CH2 domain** of the heavy chain. In contrast, for **IgM**, the binding site is located in the **CH3 domain**. This binding occurs only after the antibody has attached to an antigen, which induces a conformational change exposing these complement-binding sites. **2. Why the other options are incorrect:** * **A. VL domain (Variable Light):** This domain, along with the VH domain, forms the **paratope** (antigen-binding site). It is involved in recognizing and binding to specific epitopes, not complement. * **B. CL domain (Constant Light):** This domain provides structural support to the light chain and does not possess effector functions like complement fixation. * **C. CH1 domain (Constant Heavy 1):** This domain is part of the Fab fragment and acts as a spacer between the variable regions and the hinge region. It does not bind complement. **3. High-Yield Clinical Pearls for NEET-PG:** * **IgG Subclasses:** The efficiency of complement fixation follows the order: **IgG3 > IgG1 > IgG2**. Note that **IgG4** does not fix complement. * **IgM vs. IgG:** IgM is a more potent activator of complement than IgG because its pentameric structure provides multiple binding sites (CH3 domains) in close proximity. * **Fc Receptor Binding:** While CH2 binds complement, the **CH3 domain** of IgG is primarily responsible for binding to **Fc receptors** on phagocytic cells (opsonization) and mediating the long half-life of IgG via the neonatal Fc receptor (FcRn).

Question 306: An example of naturally acquired passive immunity is?

A. Hepatitis vaccination
B. Gamma globulin injection
C. Immune blood transfusion
D. Placental transfer of antibodies (Correct Answer)

Explanation: ### Explanation To understand this question, we must distinguish between **Natural vs. Artificial** and **Active vs. Passive** immunity. 1. **Natural vs. Artificial:** Natural occurs through biological processes (infection/maternal transfer); Artificial occurs through medical intervention (vaccines/injections). 2. **Active vs. Passive:** Active involves the body’s own immune system producing antibodies; Passive involves receiving pre-formed antibodies from another source. **Why Option D is Correct:** **Placental transfer of antibodies** (specifically IgG) is the classic example of **Naturally Acquired Passive Immunity**. It is "natural" because it occurs via a physiological process and "passive" because the fetus receives ready-made antibodies from the mother without its own immune system being stimulated. Another example is the transfer of IgA through colostrum/breast milk. **Analysis of Incorrect Options:** * **A. Hepatitis vaccination:** This is **Artificially Acquired Active Immunity**. The vaccine (antigen) is medically introduced to stimulate the individual's own immune system to produce antibodies and memory cells. * **B. Gamma globulin injection:** This is **Artificially Acquired Passive Immunity**. Pre-formed antibodies are injected (artificial) to provide immediate protection without the recipient's immune system working (passive). * **C. Immune blood transfusion:** Similar to gamma globulins, this provides pre-formed antibodies via a medical procedure, making it **Artificially Acquired Passive Immunity**. **High-Yield Clinical Pearls for NEET-PG:** * **IgG** is the only immunoglobulin that crosses the placenta (provides protection for the first 6 months of life). * **IgA** is the predominant immunoglobulin in colostrum. * **Passive Immunity** provides immediate but temporary protection (no memory). * **Active Immunity** takes time to develop but provides long-lasting protection (memory cells).

Question 307: T4 cells recognize antigen in association with all of the following EXCEPT:

A. Major histocompatibility complex class I (MHC-I) (Correct Answer)
B. MHC class II (MHC-II)
C. HLA-DR
D. HLA-DZ

Explanation: **Explanation:** The core concept tested here is the **MHC Restriction Rule**, which dictates how T-lymphocytes interact with antigens. **1. Why MHC-I is the correct answer:** T4 cells (CD4+ T-helper cells) follow the **"Rule of 8"** (4 × 2 = 8). They exclusively recognize antigens presented in association with **MHC Class II** molecules. Conversely, CD8+ T-cells (T-cytotoxic cells) recognize antigens associated with **MHC Class I** (8 × 1 = 8). Therefore, T4 cells do **not** recognize antigens via MHC-I. **2. Analysis of Incorrect Options:** * **B. MHC class II:** This is the primary molecule recognized by T4 cells. MHC-II is found on professional Antigen Presenting Cells (APCs) like macrophages, B-cells, and dendritic cells. * **C. HLA-DR:** This is a specific isotype of the human MHC Class II gene complex (along with HLA-DQ and DP). Since it is a type of MHC-II, T4 cells recognize it. * **D. HLA-DZ:** This is a lesser-known, non-classical MHC Class II sub-region. While less common in textbooks than DR/DQ, it belongs to the MHC-II family and is therefore recognized by T4 cells. **High-Yield Clinical Pearls for NEET-PG:** * **MHC-I:** Present on all nucleated cells; presents endogenous antigens (e.g., viral proteins synthesized within the cell). * **MHC-II:** Present only on APCs; presents exogenous antigens (e.g., phagocytosed bacteria). * **MHC-III:** Encodes for complement components (C2, C4) and cytokines (TNF-α), but is not involved in antigen presentation. * **Memory Hack:** CD**4** x MHC-**II** = 8; CD**8** x MHC-**I** = 8.

Question 308: Ovalbumin was injected into a rabbit. Which of the following classes of antibodies are likely to be produced initially?

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

Explanation: ### Explanation **Correct Option: C (IgE)** The correct answer is **IgE** because the question describes a classic experimental model for inducing a **Type I Hypersensitivity reaction**. Ovalbumin (a protein found in egg whites) is a potent allergen. When a foreign protein like ovalbumin is injected into an animal (like a rabbit), it acts as an allergen that triggers a Th2-mediated immune response. This leads to class-switching in B cells, specifically favoring the production of **IgE antibodies**. These IgE molecules then bind to the high-affinity FcεRI receptors on mast cells and basophils, sensitizing the animal for a subsequent allergic or anaphylactic reaction. **Why other options are incorrect:** * **IgG (Option A):** While IgG is the most abundant antibody in the secondary immune response and long-term immunity, it is not the primary antibody associated with the initial sensitization to an allergen like ovalbumin in this experimental context. * **IgM (Option B):** Although IgM is typically the first antibody produced in a *primary* immune response to general pathogens (like bacteria), the specific use of **Ovalbumin** in immunology experiments is the standard method to study **atopy and IgE production**. * **IgD (Option D):** IgD functions primarily as an antigen receptor on the surface of B cells; it is rarely secreted in significant quantities and is not the effector antibody for allergen-induced responses. --- ### High-Yield Clinical Pearls for NEET-PG * **Type I Hypersensitivity:** Mediated by IgE; involves mast cell degranulation and release of histamine. * **Prausnitz-Küstner (PK) Reaction:** An older serum transfer test used to demonstrate IgE-mediated hypersensitivity. * **Reaginic Antibody:** Another name for IgE due to its role in skin-sensitizing reactions. * **Heat Lability:** IgE is unique because it is heat-labile (destroyed at 56°C for 30 minutes), unlike IgG. * **Experimental Model:** Ovalbumin + Alum (adjuvant) is the gold standard for creating asthma/allergy models in laboratory animals.

Question 309: What is the antibacterial substance present in tears that acts by splitting cell wall components?

A. Penicillin
B. Lysozyme (Correct Answer)
C. Betalysine
D. Lactoperoxidase

Explanation: **Explanation:** The correct answer is **Lysozyme**. **1. Why Lysozyme is correct:** Lysozyme (also known as muramidase) is a key component of the innate immune system found in secretions like tears, saliva, and nasal mucus. It acts as an antibacterial agent by enzymatically cleaving the **β-1,4 glycosidic bonds** between N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) in the **peptidoglycan** layer of bacterial cell walls. This action compromises the structural integrity of the cell wall, leading to osmotic lysis of the bacteria, particularly Gram-positive organisms. **2. Why the other options are incorrect:** * **Penicillin:** While it also targets the cell wall, it is an antibiotic drug, not a naturally occurring substance in human tears. It acts by inhibiting transpeptidase enzymes (PBP) during cell wall synthesis. * **Betalysine:** This is a heat-stable substance released by platelets during coagulation. It acts primarily against Gram-positive bacteria by disrupting the cytoplasmic membrane, not by splitting the cell wall. * **Lactoperoxidase:** Found in milk and saliva, this enzyme contributes to the non-specific immune system by generating reactive oxygen species (like hypothiocyanite) that inhibit bacterial metabolism, rather than degrading the cell wall structure. **High-Yield Facts for NEET-PG:** * **Innate Immunity:** Lysozyme is a classic example of a chemical barrier in innate immunity. * **Gram-positive vs. Gram-negative:** Lysozyme is more effective against Gram-positive bacteria because their peptidoglycan layer is exposed. Gram-negative bacteria are relatively resistant due to their protective outer membrane. * **Egg White:** Alexander Fleming discovered lysozyme; it is found in high concentrations in hen egg whites.

Question 310: Which of the following is NOT an antigen-presenting cell?

A. Follicular Dendritic Cells
B. Microfold Cells (Correct Answer)
C. Mast Cells
D. Langerhans Cells

Explanation: ### Explanation The core function of an **Antigen-Presenting Cell (APC)** is to capture antigens, process them into peptides, and present them via **MHC Class II molecules** to T-lymphocytes. **Why Microfold (M) Cells are the correct answer:** M cells are specialized epithelial cells found in the **Peyer’s patches** of the intestine. Their primary role is **transcytosis**—the transport of intact antigens from the gut lumen across the epithelial barrier to underlying lymphoid tissue. Unlike true APCs, M cells **do not process antigens** or express MHC II to activate T-cells directly. They act as "gatekeepers" rather than presenters. **Analysis of other options:** * **Follicular Dendritic Cells (FDCs):** Found in B-cell follicles of secondary lymphoid organs. They trap antigen-antibody complexes via Fc receptors and present them to B-cells. (Note: They are unique as they don't always use MHC II, but are functionally classified as APCs). * **Langerhans Cells:** These are immature dendritic cells located in the **epidermis**. They are the most potent professional APCs; once they capture an antigen, they migrate to local lymph nodes to prime naive T-cells. * **Mast Cells:** Traditionally known for Type I Hypersensitivity, recent research confirms that Mast Cells can express MHC II and costimulatory molecules, allowing them to act as unconventional APCs in certain immune responses. **High-Yield Clinical Pearls for NEET-PG:** * **Professional APCs:** Dendritic cells (most potent), Macrophages, and B-cells. * **Non-Professional APCs:** Fibroblasts, Glial cells, and Vascular Endothelial cells (can present under certain cytokine influences). * **M Cells & Pathogenesis:** Certain pathogens like *Salmonella*, *Shigella*, and Poliovirus exploit M cells as a portal of entry into the systemic circulation.

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Cells and Organs of Immune System

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Antigens and Antibodies

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Major Histocompatibility Complex

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Complement System

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Cytokines and Chemokines

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Hypersensitivity Reactions

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Autoimmunity and Autoimmune Diseases

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Immunodeficiency Disorders

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Tumor Immunology

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Immunology — MCQs

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