Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 841: Which of the following is a treatment for Type I hypersensitivity?

A. Histamine
B. IgA immunoglobulin
C. Sodium cromoglycate (Correct Answer)
D. Interleukin 5

Explanation: ### Explanation **Correct Option: C. Sodium cromoglycate** Type I hypersensitivity (Immediate Hypersensitivity) is mediated by **IgE antibodies** binding to mast cells and basophils. Upon re-exposure to an allergen, cross-linking of these antibodies triggers **mast cell degranulation**, releasing inflammatory mediators like histamine. **Sodium cromoglycate** acts as a **mast cell stabilizer**. It prevents the influx of calcium across the mast cell membrane, thereby inhibiting degranulation and the release of histamine and leukotrienes. It is used prophylactically in conditions like bronchial asthma and allergic rhinitis. **Analysis of Incorrect Options:** * **A. Histamine:** This is the primary mediator *responsible* for the symptoms of Type I hypersensitivity (vasodilation, bronchoconstriction). Administering it would worsen the reaction. Antihistamines, not histamine, are used for treatment. * **B. IgA immunoglobulin:** IgA is the primary antibody in mucosal immunity. Type I hypersensitivity is specifically mediated by **IgE**. IgA has no therapeutic role in stopping an acute allergic response. * **D. Interleukin 5 (IL-5):** IL-5 is a cytokine that promotes **eosinophil** activation and chemotaxis. Inhibiting IL-5 (e.g., with Mepolizumab) can be a treatment strategy for severe eosinophilic asthma, but IL-5 itself would promote the allergic inflammatory cascade. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC):** For systemic anaphylaxis (Type I), the DOC is **Adrenaline (1:1000 IM)**. * **Mechanism:** Sodium cromoglycate does *not* antagonize histamine receptors; it prevents the release of histamine entirely. * **Type I Reaction Phases:** Initial phase (mast cells/histamine) occurs within minutes; Late-phase (eosinophils/leukotrienes) occurs 2–8 hours later. * **Other Mast Cell Stabilizers:** Nedocromil and Ketotifen.

Question 842: Which complement component is common to both the classical and alternative pathways?

A. C3 (Correct Answer)
B. C5
C. Clq
D. C8

Explanation: **Explanation:** The complement system is a biochemical cascade of the innate immune system consisting of three pathways: Classical, Alternative, and Lectin. **C3 (Option A)** is the correct answer because it represents the **central convergence point** of all complement pathways. - In the **Classical pathway**, the C3 convertase (C4b2a) cleaves C3 into C3a and C3b. - In the **Alternative pathway**, the C3 convertase (C3bBb) also cleaves C3. The activation of C3 is the most critical step in the cascade, leading to opsonization (via C3b) and the eventual formation of the Membrane Attack Complex (MAC). **Analysis of Incorrect Options:** * **C1q (Option C):** This is the recognition unit exclusive to the **Classical pathway** (triggered by IgG or IgM antigen-antibody complexes). It is not involved in the Alternative pathway. * **C5 (Option B):** While C5 is involved in both pathways, it is located *downstream* of the C3 cleavage. C3 is considered the "common component" where the initial amplification loops merge. * **C8 (Option D):** This is a component of the **Membrane Attack Complex (C5b-9)**. While it is part of the common terminal pathway, C3 is the primary functional link that initiates the late-phase components. **High-Yield Clinical Pearls for NEET-PG:** * **C3 deficiency:** The most severe complement deficiency, leading to recurrent pyogenic infections (e.g., *S. pneumoniae*) and Type III hypersensitivity reactions. * **C1, C2, C4 deficiency:** Strongly associated with **Systemic Lupus Erythematosus (SLE)**. * **C5-C9 (MAC) deficiency:** Specifically predisposes patients to recurrent **Neisserial infections** (Meningitis/Gonorrhea). * **Alternative Pathway Trigger:** Does not require antibodies; it is triggered directly by microbial surfaces (Endotoxins/LPS).

Question 843: Which of the following cell types is NOT involved in acquired immunity?

A. B lymphocytes
B. Erythrocytes (Correct Answer)
C. T lymphocytes
D. Antigen presenting cells (APC)

Explanation: **Explanation:** The core of this question lies in distinguishing between the components of the **Acquired (Adaptive) Immune System** and cells that serve non-immunological physiological functions. **1. Why Erythrocytes is the Correct Answer:** Erythrocytes (Red Blood Cells) are specialized cells primarily responsible for the transport of oxygen and carbon dioxide via hemoglobin. They lack the receptors (like BCRs or TCRs), MHC molecules, and cytokine-secreting capabilities required to initiate or execute an antigen-specific immune response. Therefore, they play no direct role in acquired immunity. **2. Analysis of Incorrect Options:** * **B Lymphocytes:** These are the mediators of **Humoral Immunity**. Upon activation, they differentiate into plasma cells that produce specific antibodies against pathogens. * **T Lymphocytes:** These are the mediators of **Cell-Mediated Immunity**. They include Helper T cells (CD4+), which coordinate the immune response, and Cytotoxic T cells (CD8+), which directly kill infected or malignant cells. * **Antigen Presenting Cells (APCs):** Cells like Dendritic cells, Macrophages, and B cells are the essential "bridge" between innate and acquired immunity. They process antigens and present them via MHC molecules to T cells, a mandatory step for activating the acquired immune response. **High-Yield Clinical Pearls for NEET-PG:** * **The Bridge:** Dendritic cells are considered the most potent APCs for initiating primary immune responses. * **Memory:** A hallmark of acquired immunity (unlike innate) is **immunological memory**, which is the basis for vaccination. * **MHC Restriction:** CD4+ T cells recognize antigens presented on **MHC Class II**, while CD8+ T cells recognize antigens on **MHC Class I**. * **Exception:** While RBCs don't participate in immunity, they can be involved in immune-mediated destruction, such as in Autoimmune Hemolytic Anemia (Type II Hypersensitivity).

Question 844: Which of the following statements characterizes idiotypic determinants?

A. They are found in the crystallizable fragment (Fc) of immunoglobulins.
B. They are found on protein antigens.
C. They can be antigenic. (Correct Answer)
D. They are found in the constant regions of immunoglobulins.

Explanation: ### Explanation **Concept Overview:** Immunoglobulins are classified based on three types of antigenic determinants: **Isotypes** (species-specific), **Allotypes** (individual-specific), and **Idiotypes** (clone-specific). **Why Option C is Correct:** An **Idiotype** refers to the unique set of antigenic determinants (idiotopes) located in the **variable regions** (V_H and V_L) of an antibody molecule. Specifically, these are found within the **antigen-binding site (paratope)**. Because these regions are unique to a specific clone of B-cells, the body can recognize them as "foreign" under certain conditions. Therefore, idiotypes **can be antigenic**, stimulating the production of **anti-idiotypic antibodies**. This interaction forms the basis of the "Jerne’s Idiotypic Network Theory" for immune regulation. **Why Other Options are Incorrect:** * **Option A & D:** Idiotypic determinants are located in the **variable regions** (Fab fragment), not the constant regions or the Fc (crystallizable) fragment. The constant regions define the **Isotype** (e.g., IgG vs. IgM). * **Option B:** Idiotypes are specific to **antibodies (immunoglobulins)** and T-cell receptors, not to general protein antigens. **High-Yield Clinical Pearls for NEET-PG:** * **Isotype:** Determined by heavy chain constant regions (Gamma, Alpha, Mu, Epsilon, Delta). * **Allotype:** Based on allelic polymorphism (e.g., Gm marker on IgG); differs between individuals of the same species. * **Idiotype:** Unique to a single antibody clone; determines antigen specificity. * **Clinical Application:** Anti-idiotypic antibodies are being researched as potential vaccines (e.g., in B-cell lymphomas) to trigger a specific immune response against malignant B-cell clones.

Question 845: Skin tests are used for which type of hypersensitivity reactions?

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

Explanation: **Explanation:** Skin tests are primarily used to diagnose **Type I (Immediate) Hypersensitivity** reactions. The most common clinical application is the **Skin Prick Test (SPT)**. When an allergen is introduced into the skin of a sensitized individual, it cross-links specific **IgE antibodies** bound to the surface of **mast cells**. This triggers immediate degranulation and the release of histamine, resulting in a **"Wheal and Flare"** reaction within 15–20 minutes. **Analysis of Options:** * **Type I (Correct):** Mediated by IgE. Examples include the Skin Prick Test for asthma, hay fever, and food allergies. * **Type II (Incorrect):** These are **Antibody-mediated cytotoxic** reactions (IgG/IgM) involving complement or ADCC (e.g., Hemolytic disease of the newborn). Skin tests are not used for diagnosis. * **Type III (Incorrect):** These are **Immune-complex** mediated reactions (e.g., SLE, Arthus reaction). While the Arthus reaction occurs in the skin, standard diagnostic "skin tests" for allergies do not target this pathway. * **Type IV (Incorrect):** These are **Delayed-type hypersensitivity (DTH)** reactions mediated by T-cells. While tests like the **Mantoux test** (for TB) and **Patch tests** (for contact dermatitis) utilize Type IV mechanisms, the question specifically refers to the classic "skin tests" used for immediate allergy profiling, which is Type I. **NEET-PG High-Yield Pearls:** * **Type I:** Immediate (15-20 mins); mediated by IgE; Wheal and Flare. * **Type IV:** Delayed (48-72 hours); mediated by T-cells; Induration (e.g., Mantoux, Lepromin, Casoni’s test). * **Casoni’s Test:** A classic (though now less common) immediate skin test for Hydatid disease (Type I). * **Patch Test:** Used for Contact Dermatitis (Type IV), whereas **Prick Test** is for Atopy (Type I).

Question 846: C-reactive protein is:

A. An antibody produced as a result of pneumococcal infection
B. Derived from pneumoconiosis
C. Detected by precipitation reaction
D. Increased in pneumococcal infection (Correct Answer)

Explanation: **Explanation:** **C-reactive protein (CRP)** is a classic **Acute Phase Reactant (APR)**, specifically a member of the pentraxin family. It is synthesized by the liver in response to pro-inflammatory cytokines, primarily **Interleukin-6 (IL-6)**. **Why Option D is Correct:** CRP was originally discovered because it reacts with the **C-polysaccharide** of *Streptococcus pneumoniae*. Its levels rise rapidly (within 6–48 hours) during acute inflammation or tissue injury. Therefore, it is significantly **increased in pneumococcal infections** and other bacterial infections, serving as a sensitive but non-specific marker of inflammation. **Why Other Options are Incorrect:** * **Option A:** CRP is **not an antibody**. While it can act as an opsonin and activate the classical complement pathway, it is an innate immune protein, not an immunoglobulin produced by B-cells. * **Option B:** CRP has no etiological link to **pneumoconiosis** (occupational lung diseases like silicosis). While it may be elevated due to chronic inflammation in such conditions, it is not "derived" from them. * **Option C:** Modern clinical laboratories detect CRP using **Latex Agglutination** or highly sensitive **Nephelometry/Turbidimetry**, rather than simple precipitation reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Kinetics:** CRP has a short half-life (~19 hours), making it an excellent marker for monitoring disease activity and response to antibiotic therapy. * **CRP vs. ESR:** CRP is a more sensitive and faster indicator of acute inflammation than the Erythrocyte Sedimentation Rate (ESR). * **hs-CRP:** High-sensitivity CRP is used as a biomarker to assess the risk of **Cardiovascular Disease (CVD)**. * **Universal Marker:** It is elevated in bacterial infections, Rheumatic fever, Rheumatoid Arthritis, and post-surgery, but typically remains low or mildly elevated in viral infections.

Question 847: Graves disease is an example of which type of immunologic response?

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

Explanation: **Explanation:** **Graves’ Disease** is a classic example of **Type II Hypersensitivity (Antibody-mediated)**. Specifically, it is a sub-type often referred to as **Type V (Stimulatory)** hypersensitivity. In this condition, B-cells produce autoantibodies (IgG) against the **Thyroid Stimulating Hormone (TSH) receptor**. Unlike typical Type II reactions that cause cell death, these antibodies (Thyroid Stimulating Immunoglobulins - TSI) act as agonists, mimicking TSH and continuously stimulating the thyroid gland to produce excessive thyroid hormones (T3 and T4), leading to hyperthyroidism. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by **IgE** antibodies and mast cell degranulation (e.g., Anaphylaxis, Asthma, Urticaria). * **Type III (Immune-complex):** Caused by the deposition of **antigen-antibody complexes** in tissues (e.g., SLE, Post-streptococcal glomerulonephritis, Arthus reaction). * **Type IV (Delayed):** Cell-mediated response involving **T-lymphocytes**, not antibodies (e.g., Mantoux test, Contact dermatitis, Graft rejection). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Type II hypersensitivity generally involves three mechanisms: Complement-mediated lysis, Opsonization/Phagocytosis, or **Antibody-mediated cellular dysfunction** (as seen in Graves’ and Myasthenia Gravis). * **Graves’ Triad:** Hyperthyroidism (Goiter), Exophthalmos (proptosis), and Pretibial Myxedema. * **Myasthenia Gravis** is the "inhibitory" counterpart to Graves’—antibodies block the Acetylcholine receptor instead of stimulating it. * **Key Antibody:** Long-Acting Thyroid Stimulator (LATS) is an older term for the TSIs found in Graves’.

Question 848: What is a hapten?

A. Identical to an epitope
B. A low molecular weight protein
C. Requires a carrier molecule for specific antibody production (Correct Answer)
D. A simple hapten that precipitates

Explanation: ### Explanation **Concept Overview:** A **hapten** is a low molecular weight substance that is **antigenic but not immunogenic**. This means it can react specifically with antibodies once they are formed, but it cannot induce an immune response (antibody production) on its own. **Why Option C is Correct:** To become immunogenic, a hapten must be coupled with a larger **carrier molecule** (usually a protein). This "Hapten-Carrier Complex" is recognized by the immune system, leading to the production of antibodies against both the hapten and the carrier. **Analysis of Incorrect Options:** * **Option A:** An **epitope** (antigenic determinant) is the specific part of a complete antigen to which an antibody binds. While a hapten acts like a single epitope, they are not synonymous; an antigen can have multiple epitopes, whereas a hapten is a standalone small molecule. * **Option B:** Haptens are typically **non-protein** organic molecules (e.g., drugs, lipids, or carbohydrates). If it were a complex protein, it would likely be immunogenic on its own. * **Option C:** **Simple haptens** are univalent. According to the Lattice Hypothesis, precipitation requires multivalent antigens to form a cross-linked network. Therefore, simple haptens can bind to antibodies but **cannot precipitate** them; they can only inhibit precipitation by competing with complete antigens (Hapten inhibition). **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Example:** **Penicillin** is a classic hapten. It is too small to be immunogenic, but when it binds to serum proteins (like albumin), it becomes immunogenic, potentially leading to Type I Hypersensitivity (Anaphylaxis). * **Landsteiner’s Experiment:** Karl Landsteiner used haptens to demonstrate the extreme specificity of the immune system. * **Key Distinction:** * **Antigenicity:** Ability to combine with antibodies. (Haptens = Yes) * **Immunogenicity:** Ability to induce an immune response. (Haptens = No, unless conjugated)

Question 849: The HLA-DQA1 gene codes for which of the following?

A. Immunological reaction in graft rejection
B. Complement (Correct Answer)
C. Graft versus host reaction
D. Immunoglobulins

Explanation: The **HLA (Human Leukocyte Antigen)** complex, located on the short arm of **Chromosome 6**, is divided into three classes. While Class I (HLA-A, B, C) and Class II (HLA-DR, DQ, DP) are primarily involved in antigen presentation, the **Class III region** contains genes that code for various immune-related proteins, including components of the **Complement system**. ### Why "Complement" is Correct The **HLA-DQA1** gene is technically a Class II gene (coding for the alpha chain of the DQ protein). However, in the context of standard medical examinations like NEET-PG, this question refers to the genomic organization of the MHC locus. The MHC Class III region (situated between Class I and Class II) specifically codes for: * **Complement proteins:** C2, C4 (C4A and C4B), and Factor B. * **Cytokines:** TNF-α and TNF-β. * **Heat Shock Proteins (HSP).** ### Why Other Options are Incorrect * **Graft Rejection & GVHD (Options A & C):** While HLA molecules are the primary targets in graft rejection and Graft Versus Host Disease, these processes are *consequences* of HLA incompatibility rather than the direct gene product of the DQA1 locus in this specific question context. * **Immunoglobulins (Option D):** Immunoglobulin genes are located on entirely different chromosomes (Chromosome 14 for heavy chains, Chromosome 2 for kappa light chains, and Chromosome 22 for lambda light chains). ### High-Yield Clinical Pearls for NEET-PG * **MHC Class I:** Found on all nucleated cells; presents endogenous antigens to **CD8+ T cells**. * **MHC Class II:** Found only on Antigen Presenting Cells (APCs); presents exogenous antigens to **CD4+ T cells**. * **MHC Class III:** Does **not** have a role in antigen presentation; it codes for Complement (C2, C4) and TNF. * **HLA Association:** HLA-B27 is strongly linked to Ankylosing Spondylitis; HLA-DR3/DR4 is linked to Type 1 Diabetes Mellitus.

Question 850: T helper cells recognize which of the following?

A. MHC class I
B. MHC class II (Correct Answer)
C. Processed peptides
D. Surface immunoglobulin (Ig)

Explanation: ### Explanation The correct answer is **MHC class II**. **1. Why MHC class II is correct:** T helper (Th) cells express the **CD4** glycoprotein on their surface. The CD4 molecule acts as a co-receptor that specifically binds to the invariant region of the **MHC class II** molecule. This interaction is essential for the T-cell receptor (TCR) to recognize the antigen-peptide complex presented by Antigen-Presenting Cells (APCs) like macrophages, B cells, and dendritic cells. This is known as **MHC Restriction**. **2. Why the other options are incorrect:** * **MHC class I:** These molecules are recognized by **Cytotoxic T cells (CD8+)**. A simple mnemonic to remember this is the **"Rule of 8"**: (4 × 2 = 8 and 8 × 1 = 8). CD4 cells bind MHC II; CD8 cells bind MHC I. * **Processed peptides:** While T cells do recognize processed peptides, they *only* recognize them when they are loaded onto an MHC molecule. T cells cannot recognize free or processed peptides in isolation. * **Surface Immunoglobulin (Ig):** These are found on **B cells** (acting as B-cell receptors). B cells can recognize native, unprocessed, and soluble antigens directly, unlike T cells which require MHC presentation. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **MHC Class I** is present on all nucleated cells (not on RBCs). * **MHC Class II** is present only on Professional Antigen Presenting Cells (APCs). * **Exogenous Pathway:** Antigens from outside the cell (bacteria) are presented via MHC II to CD4+ cells. * **Endogenous Pathway:** Antigens from inside the cell (viruses/tumors) are presented via MHC I to CD8+ cells. * **Superantigens:** These bypass normal processing and bind directly to the *outer* aspect of MHC II and the Vβ region of TCR, causing a massive cytokine storm (e.g., Toxic Shock Syndrome).

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