Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 441: Which immunoglobulins can bind complement via the classical pathway?

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

Explanation: **Explanation:** The classical pathway of the complement system is triggered by the binding of the **C1 complex** (specifically the C1q subunit) to the **Fc portion** of an antigen-antibody complex. 1. **Why IgG and IgM are correct:** * **IgM:** It is the most potent activator of the classical pathway. Being a pentamer, a single molecule of IgM bound to an antigen provides multiple Fc binding sites, easily cross-linking C1q. * **IgG:** It can activate the pathway, but requires at least two IgG molecules in close proximity to bind C1q. Among the subclasses, the order of efficiency is **IgG3 > IgG1 > IgG2**. (Note: IgG4 does not activate complement). 2. **Why other options are incorrect:** * **IgA:** It does not activate the classical pathway. However, it can activate the **Alternative pathway** (specifically secretory IgA). * **IgD and IgE:** Neither of these immunoglobulins has the structural capacity to bind C1q or initiate the complement cascade. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Classical Pathway:** "**GM** makes **C**lassic cars" (**I**g**G**, **I**g**M** activate **C**lassical). * **Alternative Pathway:** Activated by IgA, Endotoxins (LPS), and Cobra Venom Factor. * **Lectin Pathway:** Activated by Mannose-binding lectin (MBL) binding to microbial carbohydrates. * **C3b:** Acts as an opsonin (enhances phagocytosis). * **C5a:** The most potent anaphylatoxin and chemotactic agent for neutrophils. * **Membrane Attack Complex (MAC):** Composed of C5b-C9; deficiency leads to recurrent *Neisseria* infections.

Question 442: What is the term for an antigen-antibody reaction due to the presence of antibody at the surface of a cell?

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

Explanation: **Explanation:** The correct answer is **Type I hypersensitivity**. This reaction is characterized by the presence of pre-formed **IgE antibodies** bound to the surface of **mast cells and basophils** via high-affinity Fc receptors (FcεRI). When a specific antigen (allergen) cross-links these surface-bound antibodies, it triggers immediate degranulation and the release of pharmacological mediators like histamine. **Why the other options are incorrect:** * **Type II (Cytotoxic):** Here, antibodies (IgG/IgM) are directed against antigens present **on the cell surface** or extracellular matrix. The antibody is in the serum and attacks the cell; it is not "at the surface" as a receptor for the antigen. * **Type III (Immune-complex):** This involves the formation of **soluble** antigen-antibody complexes in the circulation, which later deposit in tissues (e.g., kidneys, joints) and trigger inflammation. * **Type IV (Delayed-type):** This is a **cell-mediated** response involving T-lymphocytes (Th1, Th17, or CD8+), not antibodies. **NEET-PG High-Yield Pearls:** * **Type I** is the only "Immediate" hypersensitivity; others take hours to days. * **Key Mediators:** Histamine (pre-formed), Leukotrienes (LTC4, LTD4—more potent than histamine), and Eosinophilic Chemotactic Factor (ECF-A). * **Clinical Examples:** Anaphylaxis, Atopy, Urticaria, and Extrinsic Asthma. * **PK Reaction:** The Prausnitz-Küstner reaction is a classic demonstration of Type I hypersensitivity involving the transfer of serum containing IgE.

Question 443: IgE receptors are present on which of the following cell types?

A. Mast cells (Correct Answer)
B. NK cells
C. B cells
D. Histiocytes

Explanation: **Explanation:** The correct answer is **Mast cells**. **1. Why Mast Cells are Correct:** IgE-mediated hypersensitivity (Type I) relies on the binding of IgE antibodies to high-affinity receptors known as **FcεRI**. These receptors are predominantly expressed on the surface of **mast cells** and **basophils**. When an allergen cross-links the IgE molecules already bound to these receptors, it triggers degranulation, releasing inflammatory mediators like histamine, leukotrienes, and prostaglandins. This is the fundamental mechanism behind allergic rhinitis, asthma, and anaphylaxis. **2. Why the Other Options are Incorrect:** * **NK cells:** These cells primarily express **FcγRIII (CD16)**, which binds to IgG for Antibody-Dependent Cellular Cytotoxicity (ADCC). They do not typically express IgE receptors. * **B cells:** While B cells produce IgE, they express **CD23 (FcεRII)**, a low-affinity receptor involved in regulating IgE synthesis, but they are not the primary effector cells associated with IgE-mediated clinical responses. * **Histiocytes:** These are tissue macrophages. Their primary receptors are for IgG (FcγR) and complement (C3b) to facilitate phagocytosis, rather than IgE. **Clinical Pearls for NEET-PG:** * **High-affinity receptor (FcεRI):** Found on Mast cells and Basophils. * **Low-affinity receptor (FcεRII/CD23):** Found on B cells and Eosinophils. * **Prausnitz-Küstner (PK) reaction:** A classic (though now rarely used) test demonstrating the transfer of IgE-mediated sensitivity via serum. * **Omalizumab:** A monoclonal antibody used in severe asthma that works by binding to the Fc portion of free IgE, preventing it from binding to the FcεRI on mast cells.

Question 444: Opsonisation is primarily mediated by which immunoglobulin?

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

Explanation: **Explanation:** **Opsonisation** is the process by which pathogens are coated with specific molecules (opsonins) to make them more "palatable" for phagocytosis by neutrophils and macrophages. **Why IgG is the Correct Answer:** IgG is the primary immunoglobulin responsible for opsonisation. The mechanism involves the **Fab portion** of the IgG molecule binding to specific antigens on the surface of the microbe, while the **Fc portion** binds to **Fcγ receptors** on the surface of phagocytic cells. This bridge significantly enhances the efficiency of ingestion. Specifically, **IgG1 and IgG3** are the most potent opsonins. **Analysis of Incorrect Options:** * **IgA:** Primarily involved in mucosal immunity (secretory IgA) and prevents the attachment of pathogens to epithelial surfaces. It does not act as a major opsonin. * **IgE:** Mediates type I hypersensitivity reactions (allergies) and provides immunity against helminthic parasites by activating mast cells and basophils. * **IgM:** While IgM is excellent at activating the classical complement pathway (which produces **C3b**, another potent opsonin), the IgM molecule itself does not directly opsonise because phagocytes lack specific receptors for the Fc portion of IgM. **High-Yield NEET-PG Pearls:** * **Two Major Opsonins:** The most important opsonins in the body are **IgG** (heat-stable) and **C3b** (heat-labile). * **IgG Characteristics:** It is the only antibody that crosses the placenta and is the most abundant Ig in serum. * **Complement Activation:** IgM is the most efficient antibody for complement fixation (due to its pentameric structure), but IgG is the primary direct opsonin.

Question 445: What is the main function of follicular dendritic cells?

A. To capture and present antigens to T cells
B. To capture and present antigens to B cells (Correct Answer)
C. Phagocytic activity
D. To produce immunoglobulins

Explanation: ### Explanation **Follicular Dendritic Cells (FDCs)** are unique cells located in the germinal centers of secondary lymphoid organs (lymph nodes and spleen). Unlike classical dendritic cells, FDCs are **not derived from hematopoietic stem cells**; they are of mesenchymal origin. **1. Why Option B is Correct:** The primary role of FDCs is to capture **native (unprocessed) antigens** trapped in the form of antigen-antibody complexes (immune complexes) via Fc receptors or complement receptors (C3b/C3d). They display these antigens on their surface for long periods. This allows **B cells** to recognize the antigen via their B-cell receptors (BCR), facilitating affinity maturation and the formation of memory B cells. **2. Why Other Options are Incorrect:** * **Option A:** Classical Dendritic Cells (e.g., Langerhans cells) process antigens and present them via MHC II molecules to **T cells**. FDCs do not express MHC II and do not interact primarily with T cells in this manner. * **Option C:** FDCs are **non-phagocytic**. Their function is to preserve the antigen on the cell surface rather than internalizing and digesting it. * **Option D:** Immunoglobulins are produced by **Plasma cells**, which are the terminally differentiated forms of B cells. **3. High-Yield Clinical Pearls for NEET-PG:** * **Origin:** FDCs are of **mesenchymal origin**, whereas classical DCs are of myeloid origin. * **Location:** Exclusively found in the **B-cell rich follicles** (germinal centers). * **Iccosomes:** FDCs shed small membrane-bound vesicles coated with antigens called iccosomes, which are endocytosed by B cells. * **HIV Reservoir:** FDCs are significant reservoirs for HIV; the virus particles can persist on the surface of FDCs for years, contributing to chronic infection.

Question 446: Which cells are responsible for immunity against cancer cells?

A. Basophils
B. Eosinophils
C. NK cells (Correct Answer)
D. Neutrophils

Explanation: **Explanation:** **Correct Answer: C. NK cells** Natural Killer (NK) cells are the primary mediators of **innate immunity** against intracellular pathogens and tumor cells. Unlike T-cells, they do not require prior sensitization or MHC-restricted antigen presentation. They identify cancer cells through the **"Missing Self" hypothesis**: most tumor cells downregulate MHC Class I molecules to evade T-cells. NK cells detect this absence via their **Killer Immunoglobulin-like Receptors (KIRs)**. Once activated, they induce apoptosis in cancer cells using **perforins and granzymes** and secrete **Interferon-gamma (IFN-γ)** to activate macrophages. **Why other options are incorrect:** * **A. Basophils:** These are primarily involved in Type I hypersensitivity (allergic) reactions and the release of histamine. * **B. Eosinophils:** These are specialized for defense against helminthic (parasitic) infections and play a role in allergic inflammation (e.g., asthma). * **D. Neutrophils:** These are the first responders to acute bacterial infections and are responsible for phagocytosis and NETosis, but they do not play a primary role in anti-tumor surveillance. **High-Yield Clinical Pearls for NEET-PG:** * **Markers:** NK cells are identified by the presence of **CD56 and CD16** (FcγRIII) and the absence of CD3. * **ADCC:** NK cells participate in Antibody-Dependent Cellular Cytotoxicity (ADCC) via the CD16 receptor, which binds to the Fc portion of IgG. * **IL-2 and IL-15:** These cytokines are potent stimulators of NK cell proliferation and activation. * **LAK Cells:** NK cells treated with high-dose IL-2 become Lymphokine-Activated Killer (LAK) cells, which have enhanced anti-tumor activity.

Question 447: Which of the following cytokines is not pyrogenic?

A. Interleukin-1 (IL-1)
B. Tumor Necrosis Factor-alpha (TNF-a)
C. Interleukin-4 (IL-4) (Correct Answer)
D. Interleukin-6 (IL-6)

Explanation: **Explanation:** The core concept here is the distinction between **pro-inflammatory (pyrogenic)** and **anti-inflammatory** cytokines. Pyrogens are substances that induce fever by acting on the hypothalamus to increase the set-point of body temperature, primarily through the induction of Prostaglandin E2 (PGE2). **Why Interleukin-4 (IL-4) is the correct answer:** IL-4 is a classic **anti-inflammatory cytokine** produced by Th2 cells. Its primary roles include promoting B-cell differentiation into IgE-producing plasma cells and inhibiting the production of pro-inflammatory cytokines. Because it antagonizes the inflammatory response, it does not induce fever and is therefore **not pyrogenic**. **Analysis of Incorrect Options (Pro-inflammatory Pyrogens):** * **IL-1 (Interleukin-1):** Often called the "endogenous pyrogen," it is the most potent inducer of fever. It stimulates the anterior hypothalamus to produce PGE2. * **TNF-α (Tumor Necrosis Factor-alpha):** A major mediator of acute inflammation and septic shock. It induces fever both directly and by stimulating the release of IL-1. * **IL-6 (Interleukin-6):** A key mediator of the acute-phase response. It acts as a pyrogen and is the primary stimulus for the liver to produce C-reactive protein (CRP). **High-Yield Clinical Pearls for NEET-PG:** * **Endogenous Pyrogens:** IL-1, IL-6, TNF-α, and IFN-γ. * **Exogenous Pyrogen:** Lipopolysaccharide (LPS) from Gram-negative bacteria is the most common example; it triggers the release of endogenous pyrogens. * **Mechanism of Fever:** Cytokines → Hypothalamic vascular endothelium → COX-2 activation → PGE2 release → Increased thermoregulatory set-point. * **Anti-inflammatory Cytokines:** IL-4, IL-10, and TGF-β (Think: "IL-10 and 4 keep the inflammation on the floor").

Question 448: Which complement component binds with the Fc portion of IgM in the classical pathway?

A. C1 (Correct Answer)
B. C2
C. C3
D. C4

Explanation: **Explanation:** The **Classical Pathway** of the complement system is initiated by the binding of the **C1 complex** to the Fc portion of an antigen-antibody complex. 1. **Why C1 is correct:** The C1 complex (specifically the **C1q** subunit) has receptors for the **CH2 domain of IgG** and the **CH3 domain of IgM**. IgM is a pentamer, making it a highly efficient activator of the classical pathway because a single IgM molecule can provide the multiple binding sites required for C1q to attach and become activated. Once C1q binds, it activates C1r and C1s, which then proceed to cleave C4 and C2. 2. **Why other options are incorrect:** * **C4 and C2:** These are substrates for the activated C1s enzyme. C1s cleaves C4 into C4a and C4b, and C2 into C2a and C2b. They do not bind directly to the antibody. * **C3:** This is the most abundant complement protein and the point where all three pathways (Classical, Alternative, and Lectin) converge. It is cleaved by **C3 convertase** (C4b2a in the classical pathway), not by the antibody itself. **High-Yield Clinical Pearls for NEET-PG:** * **Order of activation:** C1 → C4 → C2 → C3 → C5-C9. (Note: C4 comes before C2). * **IgM vs. IgG:** IgM is the most potent activator of the classical pathway ("**M**ighty" activator). Among IgG subclasses, the order of efficiency is **IgG3 > IgG1 > IgG2**. IgG4 does not activate the classical pathway. * **Calcium Dependency:** The C1 complex (C1qrs) is stabilized by **Calcium ions**. * **C1 Esterase Inhibitor deficiency:** Leads to **Hereditary Angioedema** due to over-activation and consumption of C4 and C2.

Question 449: NK cells express which of the following surface markers?

A. CD15, CD55
B. CD16, CD56 (Correct Answer)
C. CD16, CD57
D. CD21, CD66

Explanation: **Explanation:** Natural Killer (NK) cells are large granular lymphocytes that play a critical role in the innate immune system. They are unique because they can destroy virally infected or tumor cells without prior sensitization. **Why Option B is Correct:** The definitive surface markers for identifying NK cells are **CD16** and **CD56**. * **CD16 (FcγRIII):** This is a low-affinity receptor for the Fc portion of IgG. It allows NK cells to bind to antibody-coated target cells and destroy them via **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. * **CD56 (NCAM):** An adhesion molecule used as the primary marker for NK cell identification in flow cytometry. **Analysis of Incorrect Options:** * **Option A (CD15, CD55):** CD15 is a marker for **Granulocytes** (Neutrophils) and Reed-Sternberg cells. CD55 (DAF) is a complement regulatory protein found on all blood cells. * **Option C (CD16, CD57):** While CD57 can be expressed on mature NK cells, it is not as specific or universal as CD56 for diagnostic identification. * **Option D (CD21, CD66):** CD21 (CR2) is the receptor for the **Epstein-Barr Virus (EBV)** and is found on **B-cells**. CD66 is a marker for neutrophils. **High-Yield Clinical Pearls for NEET-PG:** 1. **MHC-I Rule:** NK cells kill cells that lack **MHC Class I** molecules (the "Missing Self" hypothesis). 2. **Cytokines:** NK cell activity is stimulated by **IL-2, IL-12, and IFN-α/β**. 3. **Chediak-Higashi Syndrome:** Characterized by a functional defect in NK cells, leading to recurrent infections. 4. **Markers:** NK cells are **CD3 negative** (unlike T-cells). The presence of CD3 and CD56 together indicates NKT cells.

Question 450: Which of the following is a screening test for cell defects?

A. Isohemagglutinin titers (Correct Answer)
B. CD4 levels
C. Nitroblue tetrazolium dye test
D. Candida albicans intradermal skin test

Explanation: **Explanation:** The question asks for a screening test for **B-cell (humoral) defects**. **1. Why Isohemagglutinin titers are correct:** Isohemagglutinins (Anti-A and Anti-B) are naturally occurring **IgM antibodies** produced against gut flora that cross-react with ABO blood group antigens. Since these are produced without active immunization, measuring their titers is a standard, cost-effective **screening test** to assess a patient's ability to produce functional antibodies (humoral immunity). A low or absent titer in a patient older than 6 months (after maternal antibodies wane) suggests a B-cell defect or hypogammaglobulinemia. **2. Analysis of Incorrect Options:** * **CD4 levels (Option B):** This is a quantitative test for **T-cells**, typically used to monitor HIV progression. While it assesses cellular immunity, it is not a screening test for B-cell defects. * **Nitroblue tetrazolium (NBT) dye test (Option C):** This is the classic screening test for **Chronic Granulomatous Disease (CGD)**, which is a defect in **phagocytic function** (specifically the NADPH oxidase enzyme), not B-cells. * **Candida albicans intradermal skin test (Option D):** This is a Delayed-Type Hypersensitivity (DTH) test used to screen for **T-cell (cell-mediated) immunity** defects. A positive skin wheal indicates functional T-cells and macrophages. **Clinical Pearls for NEET-PG:** * **B-cell Screening:** Total IgG/IgA/IgM levels, Isohemagglutinin titers, and Schick test. * **T-cell Screening:** Absolute lymphocyte count, Chest X-ray (for Thymic shadow in infants), and DTH skin tests. * **Phagocytic Screening:** NBT test or Dihydrorhodamine (DHR) flow cytometry. * **Complement Screening:** CH50 assay.

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