Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 331: The Fernandez reaction in the lepromin test is a type of?

A. Type 1 Hypersensitive reaction
B. Type 2 Hypersensitive reaction
C. Type 3 Hypersensitive reaction
D. Type 4 Hypersensitive reaction (Correct Answer)

Explanation: ### Explanation The **Lepromin test** is a skin test used to determine the cell-mediated immunity (CMI) of a patient against *Mycobacterium leprae*. It involves two distinct clinical readings: the **Fernandez reaction** and the **Mitsuda reaction**. **Why Option D is Correct:** The Fernandez reaction is an early response read at **48–72 hours**. It is a classic example of a **Type 4 (Delayed-type) Hypersensitivity reaction**. It occurs due to the infiltration of sensitized T-lymphocytes and macrophages at the site of lepromin injection, indicating prior exposure to the leprosy bacillus. (Note: The Mitsuda reaction, read at 3–4 weeks, is also a Type 4 reaction but signifies a granulomatous response). **Why Other Options are Incorrect:** * **Option A (Type 1):** These are immediate reactions mediated by **IgE antibodies** and mast cell degranulation (e.g., Anaphylaxis, Asthma). The Fernandez reaction takes days, not minutes, to develop. * **Option B (Type 2):** These are **cytotoxic reactions** where antibodies (IgG/IgM) react with antigens on cell surfaces (e.g., ABO incompatibility). * **Option C (Type 3):** These are **immune-complex mediated** reactions (e.g., Arthus reaction, Serum sickness). While Type 3 reactions can occur in leprosy (specifically **Erythema Nodosum Leprosum** or Type 2 Lepra reaction), they do not define the Fernandez reaction. **High-Yield Clinical Pearls for NEET-PG:** * **Fernandez Reaction:** Read at 48–72 hours (Early). * **Mitsuda Reaction:** Read at 21 days/3 weeks (Late). It is more clinically significant as it correlates with the patient's prognosis and helps classify the type of leprosy. * **Prognostic Value:** The Lepromin test is **positive** in Tuberculoid Leprosy (strong CMI) and **negative** in Lepromatous Leprosy (weak CMI). * **Diagnostic Value:** It is **NOT** used to diagnose leprosy; it is used for classification and prognosis.

Question 332: Which of the following immunoglobulins does not fix complement?

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

Explanation: **Explanation:** The ability of an immunoglobulin to "fix complement" refers to its capacity to initiate the **Classical Pathway** of the complement system. This process begins when the C1q component binds to the Fc portion of an antibody that is already bound to an antigen. **Why IgE is the correct answer:** **IgE** (along with IgD) does not possess the specific binding sites on its Fc region required to activate the classical complement pathway. Its primary physiological role is mediating Type I hypersensitivity reactions (allergy) and providing defense against helminthic infections by binding to mast cells and basophils via high-affinity FcεRI receptors. **Analysis of incorrect options:** * **IgM:** This is the **most potent** activator of the classical pathway. Due to its pentameric structure, a single molecule of IgM can provide the multiple Fc binding sites necessary for C1q attachment. * **IgG:** This is a strong complement fixer. Among its subclasses, the order of efficiency is **IgG3 > IgG1 > IgG2**. Note that **IgG4** does not fix complement. * **IgA:** While IgA does not activate the *classical* pathway, it can activate the **Alternative Pathway** (especially in its secretory or aggregated form). However, in the context of standard NEET-PG questions regarding "complement fixation" (which implies the classical pathway), IgE and IgD are the definitive "non-fixers." **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Classical Pathway Fixation:** **"GM Makes Classic cars"** (Ig**G** and Ig**M** activate the **Classic**al pathway). * **Alternative Pathway:** Activated by IgA, Endotoxins, and Cobra Venom Factor. * **IgG Subclass Exception:** Remember that **IgG4** is the only IgG subclass that does not fix complement. * **Valency:** IgM is a pentamer (valency of 10), making it the most efficient at agglutination and complement fixation.

Question 333: Which of the following cell types is thought to function in suppressing the immune response?

A. Inducible T reg cells (Correct Answer)
B. B cells
C. T memory cells
D. TH cells

Explanation: **Explanation:** The correct answer is **Inducible T reg cells (A)**. Regulatory T cells (Tregs) are a specialized subpopulation of T cells that act as the "brakes" of the immune system. Their primary function is to maintain self-tolerance and prevent autoimmune diseases by suppressing the activation and proliferation of effector T cells (like TH and TC cells). Tregs are classified into two types: 1. **Natural Tregs (nTregs):** Develop in the thymus. 2. **Inducible/Adaptive Tregs (iTregs):** Develop in the periphery from mature CD4+ T cells under the influence of cytokines like TGF-β. Both types typically express the transcription factor **FoxP3** and surface markers **CD4 and CD25**. **Why other options are incorrect:** * **B cells:** These are mediators of humoral immunity. Upon activation, they differentiate into plasma cells to produce antibodies; they do not primarily function to suppress the immune response. * **T memory cells:** These are long-lived cells formed after an initial exposure to an antigen. They provide a rapid and heightened secondary immune response upon re-exposure. * **TH cells (Helper T cells):** These cells (CD4+) orchestrate the immune response by secreting cytokines that activate B cells, cytotoxic T cells, and macrophages. They enhance rather than suppress the immune response. **High-Yield Clinical Pearls for NEET-PG:** * **IPEX Syndrome:** Caused by a mutation in the **FoxP3 gene**, leading to a deficiency of Tregs. It presents with the triad of Immune dysregulation, Polyendocrinopathy, and Enteropathy. * **Cytokine Profile:** Tregs suppress the immune system by secreting inhibitory cytokines, specifically **IL-10** and **TGF-β**. * **Marker:** CD25 is the alpha chain of the IL-2 receptor, which is constitutively expressed on Tregs.

Question 334: The term epitope refers to which part of an antigen?

A. The complete antigen molecule
B. A hapten
C. An immunogen
D. The smallest antigenic determinant (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. The smallest antigenic determinant** An **epitope** (also known as an antigenic determinant) is the specific chemical group or site on an antigen molecule that is physically recognized and bound by an antibody or a T-cell receptor. Antigens are typically large macromolecules, but the immune system does not react to the entire molecule at once; instead, it targets these discrete, small regions (usually 5–15 amino acids or sugar residues). #### Analysis of Incorrect Options: * **A. The complete antigen molecule:** An antigen is the entire substance (e.g., a protein or polysaccharide) capable of being bound by an antibody. One antigen can possess multiple different epitopes (multivalent), allowing different antibodies to bind simultaneously. * **B. A hapten:** A hapten is a small molecule that is antigenic (can bind to antibodies) but **not immunogenic** on its own. It only induces an immune response when conjugated to a larger carrier protein. * **C. An immunogen:** This is a substance capable of inducing a specific immune response. While all immunogens are antigens, not all antigens are immunogens (e.g., haptens). #### High-Yield Clinical Pearls for NEET-PG: * **Paratope:** This is the corresponding antigen-binding site on the **antibody** (the "lock" to the epitope's "key"). * **T-cell vs. B-cell Epitopes:** B-cell epitopes can be **conformational** (dependent on 3D folding) or linear. T-cell epitopes are always **linear** peptides, as they must be processed and presented on MHC molecules. * **Adjuvant:** A substance added to vaccines to enhance the immunogenicity of an antigen without being an antigen itself (e.g., Alum).

Question 335: Which of the following statements is true about a hapten?

A. It induces a brisk immune response.
B. It needs a carrier to induce an immune response. (Correct Answer)
C. It is a T-independent antigen.
D. It has no association with MHC.

Explanation: ### Explanation **Correct Answer: B. It needs a carrier to induce an immune response.** A **hapten** is a small molecule that is **antigenic but not immunogenic**. This means it can react specifically with antibodies once they are formed, but it cannot initiate an immune response on its own. To become immunogenic, a hapten must covalently bind to a larger protein molecule known as a **carrier**. Once the hapten-carrier complex is formed, the immune system recognizes it as a foreign entity and produces antibodies against both the hapten and the carrier. #### Analysis of Incorrect Options: * **A. It induces a brisk immune response:** Incorrect. By definition, a hapten is non-immunogenic. It lacks the complexity and molecular weight required to stimulate B or T cells independently. * **C. It is a T-independent antigen:** Incorrect. Haptens typically require the carrier protein to be processed and presented via the **MHC-II pathway** to T-helper cells. Therefore, the response to a hapten-carrier complex is T-cell dependent. * **D. It has no association with MHC:** Incorrect. While the hapten itself doesn't bind MHC, the carrier protein it attaches to is processed into peptides and presented on MHC molecules to activate T-cells, which then provide "help" to B-cells to produce anti-hapten antibodies. #### High-Yield Clinical Pearls for NEET-PG: * **Landsteiner’s Experiment:** Karl Landsteiner is credited with the discovery of haptens. * **Clinical Example (Drug Allergy):** Penicillin is a classic hapten. It is too small to be immunogenic, but it binds to serum proteins (like albumin) to form a complex that triggers Type I Hypersensitivity (Anaphylaxis). * **Poison Ivy:** Urushiol (the toxin in poison ivy) acts as a hapten that binds to skin proteins, leading to a Type IV Hypersensitivity (Contact Dermatitis). * **Key Distinction:** * **Antigenicity:** Ability to combine with antibodies. * **Immunogenicity:** Ability to induce an immune response. (Haptens have the former, but lack the latter).

Question 336: Which of the following statements is true regarding Toll-like receptors?

A. Antigen specific
B. Acts by cytokine release
C. Part of adaptive immunity
D. Part of innate immunity (Correct Answer)

Explanation: ### Explanation **Toll-like Receptors (TLRs)** are a class of **Pattern Recognition Receptors (PRRs)** that play a pivotal role in the body's first line of defense. **Why Option D is correct:** TLRs are fundamental components of **Innate Immunity**. They are evolutionarily conserved receptors expressed on sentinel cells like macrophages and dendritic cells. They recognize highly conserved microbial structures known as **Pathogen-Associated Molecular Patterns (PAMPs)**—such as LPS, flagellin, or viral RNA—allowing the immune system to detect the presence of "non-self" immediately upon entry, without prior exposure. **Why other options are incorrect:** * **Option A & C:** TLRs are **not antigen-specific** and are not part of adaptive immunity. Unlike B-cell or T-cell receptors, which undergo genetic rearrangement to recognize specific unique epitopes, TLRs have broad specificity for entire classes of microbes. * **Option B:** While TLR activation *leads* to the production of cytokines (via the NF-κB pathway), the receptors themselves do not "act by cytokine release." They act by **ligand binding and signal transduction**. Cytokine release is the *result* of TLR activation, not the mechanism of the receptor itself. --- ### High-Yield Facts for NEET-PG * **Location:** TLRs can be **extracellular** (TLR 1, 2, 4, 5, 6—detecting bacteria/fungi) or **endosomal** (TLR 3, 7, 8, 9—detecting nucleic acids/viruses). * **Key TLRs to Remember:** * **TLR-4:** Recognizes **Lipopolysaccharide (LPS)** of Gram-negative bacteria (associated with septic shock). * **TLR-2:** Recognizes Peptidoglycan/Teichoic acid (Gram-positive bacteria). * **TLR-3:** Recognizes dsRNA. * **TLR-5:** Recognizes Flagellin. * **TLR-9:** Recognizes unmethylated CpG DNA. * **Adapter Protein:** Most TLRs (except TLR-3) utilize the **MyD88** signaling pathway to activate NF-κB.

Question 337: In ataxia-telangiectasia, which immunoglobulin is absent?

A. IgG
B. IgM
C. IgA (Correct Answer)
D. Abnormal structure of IgA

Explanation: **Explanation:** **Ataxia-Telangiectasia (AT)** is an autosomal recessive multisystem disorder caused by a mutation in the **ATM (Ataxia-Telangiectasia Mutated) gene** on chromosome 11. This gene is responsible for repairing double-stranded DNA breaks. **Why IgA is the correct answer:** The defect in DNA repair leads to impaired **class-switch recombination**, which is essential for producing different immunoglobulin isotypes. In AT, the most common and characteristic immunologic finding is a **selective deficiency of IgA** (seen in about 70% of patients). While IgG subclasses (IgG2/IgG4) and IgE may also be low, the complete absence or profound deficiency of IgA is the classic diagnostic hallmark mentioned in high-yield medical literature. **Analysis of Incorrect Options:** * **IgG:** While IgG levels can be low (hypogammaglobulinemia) in some patients, it is rarely completely absent. * **IgM:** IgM levels are typically **normal or even elevated** in AT because the defect lies in switching *away* from IgM to other classes. * **Abnormal structure of IgA:** The pathology in AT is a quantitative failure of production (deficiency), not a qualitative defect in the molecular structure of the immunoglobulin itself. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Cerebellar ataxia (early childhood), Oculocutaneous telangiectasia (spider veins in eyes/skin), and recurrent sinopulmonary infections. * **Laboratory Marker:** Characteristically **elevated Alpha-Fetoprotein (AFP)** levels in children >1 year old. * **Complications:** High risk of malignancies (Lymphomas and Leukemias) and extreme sensitivity to ionizing radiation (X-rays/CT scans).

Question 338: Which of the following is NOT a costimulatory factor for T cells?

A. B7-1
B. B7-2
C. B7-3 (Correct Answer)
D. CD40

Explanation: **Explanation:** T-cell activation requires a **"Two-Signal Model"** to prevent inappropriate immune responses. Signal 1 is the recognition of the Antigen-MHC complex by the T-cell receptor (TCR). Signal 2 is the **costimulatory signal**, provided by the interaction between molecules on the Antigen Presenting Cell (APC) and the T-cell. **Why C is the Correct Answer:** There are two primary members of the B7 family involved in T-cell costimulation: **B7-1 (CD80)** and **B7-2 (CD86)**. **B7-3 does not exist** as a recognized costimulatory molecule in standard human immunology, making it the "except" in this list. **Analysis of Incorrect Options:** * **A & B (B7-1 and B7-2):** These are expressed on professional APCs (dendritic cells, macrophages, B cells). They bind to **CD28** on the T-cell to provide the essential second signal for activation and IL-2 production. * **D (CD40):** While CD40 (on APCs) binds to CD40L (on T-cells), it is a critical costimulatory pathway. This interaction "licenses" the APC to express more B7-1/B7-2 and is vital for B-cell class switching and macrophage activation. **High-Yield NEET-PG Pearls:** * **Anergy:** If Signal 1 occurs without Signal 2 (costimulation), the T-cell becomes non-responsive (anergic). * **CTLA-4:** This molecule on T-cells binds to B7-1/2 with higher affinity than CD28 but sends an **inhibitory** signal, acting as a "brake" on the immune system (Target of Abatacept). * **PD-1:** Another inhibitory checkpoint; its blockade is a major target in cancer immunotherapy (e.g., Pembrolizumab).

Question 339: What is the primary function of a plasma cell?

A. Cell-mediated immunity (CMI)
B. Phagocytosis
C. Opsonization
D. Antibody formation (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Antibody formation** Plasma cells are the terminal differentiation stage of **B-lymphocytes**. When a B-cell encounters its specific antigen and receives T-cell help, it undergoes clonal expansion and matures into a plasma cell. These cells are essentially "antibody factories"; they possess an extensive rough endoplasmic reticulum (RER) and a prominent Golgi apparatus, specialized for the large-scale synthesis and secretion of **immunoglobulins (antibodies)** into the blood and lymph. **Analysis of Incorrect Options:** * **A. Cell-mediated immunity (CMI):** This is the primary function of **T-lymphocytes** (specifically CD8+ cytotoxic T-cells and CD4+ helper T-cells), not B-cells or plasma cells. * **B. Phagocytosis:** This is the process of engulfing and destroying pathogens, performed by professional phagocytes such as **neutrophils, macrophages, and dendritic cells**. * **C. Opsonization:** While antibodies produced by plasma cells *act* as opsonins (tagging pathogens for destruction), the act of opsonization itself is a process involving the coating of an antigen. The plasma cell’s primary biological role is the **production** of the molecules that perform this task. **High-Yield NEET-PG Pearls:** * **Morphology:** Plasma cells exhibit a characteristic **"Cart-wheel" or "Clock-face" appearance** of the nucleus due to clumps of heterochromatin. * **Perinuclear Halo:** They often show a clear zone near the nucleus (perinuclear hof), which represents the large Golgi apparatus. * **Russell Bodies:** These are eosinophilic inclusions found in plasma cells representing overloaded immunoglobulin deposits. * **Clinical Correlation:** **Multiple Myeloma** is a plasma cell dyscrasia characterized by the malignant proliferation of a single clone of plasma cells, leading to the production of monoclonal (M) proteins.

Question 340: Which immune cells have CD16 and CD56 on their surface and are important in immunological surveillance and defense against virus-infected and malignant cells?

A. Helper T-cells
B. Dendritic cells
C. Natural killer cells (Correct Answer)
D. Macrophages

Explanation: ### Explanation **Correct Answer: C. Natural killer cells** **Underlying Medical Concept:** Natural Killer (NK) cells are large granular lymphocytes that form a critical part of the **innate immune system**. They are uniquely identified by the presence of **CD56** (NCAM - Neural Cell Adhesion Molecule) and **CD16** (FcγRIII). * **CD16** allows NK cells to bind to the Fc portion of IgG, mediating **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. * **Function:** They provide the first line of defense against intracellular pathogens (viruses) and tumor cells. Unlike T-cells, they do not require prior sensitization or MHC-restriction; they kill cells that show "missing self" (downregulated MHC-I expression). **Analysis of Incorrect Options:** * **A. Helper T-cells:** These are characterized by **CD3** and **CD4** markers. They recognize antigens presented on MHC-II and coordinate the adaptive immune response rather than providing non-specific surveillance. * **B. Dendritic cells:** These are professional Antigen-Presenting Cells (APCs) characterized by markers like **CD11c** and **HLA-DR**. Their primary role is to process and present antigens to T-cells, not direct cytotoxicity. * **D. Macrophages:** While they are part of innate immunity, their primary markers are **CD14** and **CD64**. They function via phagocytosis and cytokine production rather than the CD16/56-mediated killing mechanism. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Markers:** CD16, CD56, and **CD94**. They are **CD3 negative**. * **Mechanism of Killing:** Release of **Perforins** (create pores) and **Granzymes** (induce apoptosis). * **Cytokine Activation:** NK cell activity is significantly enhanced by **IL-2, IL-12, and IFN-α/β**. * **Clinical Correlation:** Deficiency in NK cell function leads to recurrent viral infections (especially Herpesviridae) and increased susceptibility to malignancies.

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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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Immunology — MCQs

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