Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 451: Which immunoglobulin has the maximum molecular weight and is the first to be synthesized in a fetus?

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

Explanation: **Explanation:** **IgM** is the correct answer because it is a **pentamer** in its secreted form, consisting of five basic units joined by a J-chain. This pentameric structure gives it a molecular weight of approximately **900,000 Daltons (900 kDa)**, making it the largest of all immunoglobulins (often called the "millionaire molecule"). Furthermore, IgM is the first immunoglobulin class to be synthesized by the fetus (starting around 20 weeks of gestation). Its presence in cord blood or a neonate indicates an intrauterine infection (e.g., TORCH), as maternal IgM cannot cross the placenta. **Why other options are incorrect:** * **IgA:** Primarily found in secretions (as a dimer). Its molecular weight is ~160–385 kDa. It provides mucosal immunity and is the most abundant Ig in breast milk (colostrum). * **IgG:** The most abundant Ig in serum and the only one that **crosses the placenta**. However, it is a monomer with a low molecular weight (~150 kDa). Fetal IgG is primarily maternal in origin. * **IgD:** Found on the surface of B-cells as a receptor; it has a low serum concentration and a molecular weight of ~180 kDa. **High-Yield NEET-PG Pearls:** * **Valency:** IgM has a theoretical valency of 10 (highest), though it usually binds 5 antigens due to steric hindrance. * **Complement Activation:** IgM is the most efficient immunoglobulin at activating the classical complement pathway. * **Half-life:** IgG has the longest half-life (23 days), while IgM has a half-life of about 5 days. * **Agglutination:** Due to its size and valency, IgM is the most effective antibody for agglutination and cytolysis.

Question 452: Immune complex mediated hypersensitivity reaction is:

A. Type-1 hypersensitivity
B. Type-2 hypersensitivity
C. Type-3 hypersensitivity (Correct Answer)
D. Type-4 hypersensitivity

Explanation: **Explanation:** **Type-3 Hypersensitivity (Correct Answer):** Type-3 hypersensitivity is characterized by the formation of **antigen-antibody (immune) complexes**. These complexes circulate in the blood and eventually deposit in various tissues (like blood vessel walls, synovial membranes, or glomerular basements). Once deposited, they activate the **classical complement pathway**, leading to the recruitment of neutrophils, release of lysosomal enzymes, and subsequent tissue damage (vasculitis). **Why other options are incorrect:** * **Type-1 (Immediate):** Mediated by **IgE antibodies** binding to mast cells and basophils. It involves the release of histamine and is seen in anaphylaxis and asthma. * **Type-2 (Cytotoxic):** Mediated by **IgG or IgM** antibodies directed against antigens on **specific cell surfaces** or tissues (e.g., ABO incompatibility, Myasthenia Gravis). * **Type-4 (Delayed):** The only **cell-mediated** hypersensitivity. It involves T-lymphocytes (CD4+ or CD8+) rather than antibodies. Examples include the Mantoux test and contact dermatitis. **NEET-PG High-Yield Pearls:** * **Mnemonic (ACID):** **A**naphylactic (Type 1), **C**ytotoxic (Type 2), **I**mmune-Complex (Type 3), **D**elayed (Type 4). * **Classic Examples of Type-3:** Systemic Lupus Erythematosus (SLE), Post-Streptococcal Glomerulonephritis (PSGN), Rheumatoid Arthritis, and **Serum Sickness** (systemic) or **Arthus Reaction** (local). * **Key Mediator:** Complement activation (C3a, C4a, C5a) and Neutrophils are the primary effectors of damage in Type-3 reactions.

Question 453: Which of the following is NOT a function of the complement system?

A. Chemotaxis
B. Opsonization
C. Cell lysis
D. Antigen presentation (Correct Answer)

Explanation: The complement system is a crucial component of the innate immune system consisting of plasma proteins that "complement" the ability of antibodies and phagocytic cells to clear pathogens. ### **Why Antigen Presentation is the Correct Answer** **Antigen presentation** is a function of specialized cells known as **Antigen-Presenting Cells (APCs)**, such as dendritic cells, macrophages, and B-cells. These cells process pathogens and display their peptides on **MHC molecules** to T-cells. The complement system consists of soluble proteins and does not possess the cellular machinery required to process or present antigens. ### **Analysis of Incorrect Options** * **A. Chemotaxis:** Small fragments like **C5a** (and to a lesser extent C3a and C4a) act as potent chemoattractants. C5a specifically recruits and activates neutrophils and macrophages to the site of inflammation. * **B. Opsonization:** **C3b** (and iC3b) acts as an opsonin. It coats the surface of bacteria, making them easily "recognizable" and "tasty" for phagocytes which possess CR1 receptors. * **C. Cell Lysis:** The final step of the complement cascade is the formation of the **Membrane Attack Complex (MAC)**, composed of **C5b-C9**. This complex creates pores in the lipid bilayer of pathogens, leading to osmotic lysis. ### **High-Yield Clinical Pearls for NEET-PG** * **C3b** = **B**inds Bacteria (**Opsonization**). * **C3a, C4a, C5a** = **A**naphylatoxins (trigger mast cell degranulation). * **C5a** = Neutrophil **C**hemotaxis. * **Deficiency of C1-C4:** Associated with Systemic Lupus Erythematosus (**SLE**). * **Deficiency of C5-C9:** Increases susceptibility to **Neisseria** infections. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Caused by a deficiency of DAF (CD55) and MIRL (CD59), which normally protect host cells from complement-mediated lysis.

Question 454: Job syndrome is due to what defect?

A. Defect in chemotaxis
B. Defect in phagocytosis (Correct Answer)
C. Defect in synthesis
D. Defect in leukocyte function

Explanation: **Explanation:** **Job Syndrome (Hyper-IgE Syndrome)** is a primary immunodeficiency disorder characterized by a triad of high serum IgE levels, recurrent "cold" staphylococcal abscesses, and chronic eczema. **Why Option B is correct:** The fundamental defect in Job Syndrome is a mutation in the **STAT3 gene**, which leads to a failure of Th17 cell differentiation. This results in a deficiency of IL-17. Since IL-17 is crucial for the recruitment and activation of neutrophils, its absence leads to a **defect in phagocytosis** (specifically, the inability of neutrophils to reach the site of infection and effectively clear pathogens). This impaired phagocytic response is why patients develop "cold" abscesses—infections that lack the typical signs of inflammation like heat or redness. **Why other options are incorrect:** * **Option A (Chemotaxis):** While neutrophil migration is impaired, the primary classification in standard textbooks (like Ananthanarayan) often groups Job syndrome under functional defects of phagocytes. Pure chemotactic defects are more classically associated with **LAD (Leukocyte Adhesion Deficiency)**. * **Option C (Synthesis):** This is a vague term. Job syndrome involves a signaling defect (STAT3), not a primary failure in the synthesis of immunoglobulins (in fact, IgE synthesis is pathologically increased). * **Option D (Leukocyte function):** This is a broad category. While technically true, "Defect in phagocytosis" is the more specific and clinically accurate description of the functional failure in this syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most commonly Autosomal Dominant (STAT3 mutation). * **Clinical Triad:** "F-A-S-T-E" – **F**acial features (coarse), **A**bscesses (cold), **S**hedding of primary teeth (delayed), **T**h17 deficiency, **E**levated IgE. * **Laboratory:** Serum IgE levels often exceed **2000 IU/ml**. * **Pathogen:** Most common infecting organism is *Staphylococcus aureus*.

Question 455: Which Interleukin activates eosinophils?

A. IL-1
B. IL-4
C. IL-5 (Correct Answer)
D. IL-6

Explanation: ### Explanation **Correct Answer: C. IL-5** **Mechanism and Concept:** Interleukin-5 (IL-5) is a key cytokine produced primarily by **Th2 cells** and Group 2 Innate Lymphoid Cells (ILC2s). It is the most specific cytokine for eosinophil lineage. Its primary functions include: 1. **Production:** Stimulating the bone marrow to produce eosinophils (eosinopoiesis). 2. **Activation:** Enhancing the effector functions of eosinophils, such as degranulation. 3. **Recruitment:** Promoting the migration and survival of eosinophils at sites of helminthic infections and allergic inflammation. **Analysis of Incorrect Options:** * **A. IL-1:** Produced by macrophages; it is a pro-inflammatory cytokine responsible for inducing **fever** (endogenous pyrogen) and activating vascular endothelium. * **B. IL-4:** Also produced by Th2 cells, but its primary role is inducing **B-cell class switching to IgE** and promoting Th2 differentiation. While it supports the allergic response, it does not directly activate eosinophils. * **D. IL-6:** An acute-phase reactant stimulator. It triggers the liver to produce proteins like CRP and plays a role in B-cell differentiation into plasma cells. **NEET-PG High-Yield Pearls:** * **Mnemonic for Th2 Cytokines:** "IL-**4**, **5**, and **6**." * **IL-4:** Stimulates Ig**E** (4 looks like E). * **IL-5:** Stimulates **E**osinophils (5 looks like S in Eosinophil**s**). * **Clinical Correlation:** Monoclonal antibodies targeting IL-5 (e.g., **Mepolizumab**, **Reslizumab**) or its receptor (**Benralizumab**) are used in the treatment of severe eosinophilic asthma. * **Eosinophilia:** Classically seen in **N**eoplasia, **A**llergy, **A**sthma, **C**onnective tissue diseases, and **P**arasites (Mnemonic: **NAACP**).

Question 456: Which of the following is true about cytokines?

A. Cytokines are always polypeptides. (Correct Answer)
B. Cytokines act on protein targets.
C. Cytokines participate in intrinsic enzymatic reactions.
D. Cytokines are involved in chemotaxis.

Explanation: ### Explanation **1. Why Option A is Correct:** Cytokines are a broad category of small, soluble **polypeptides** (proteins or glycoproteins) produced by a wide variety of cells (e.g., macrophages, lymphocytes, mast cells). They function as chemical messengers that mediate and regulate immunity, inflammation, and hematopoiesis. Unlike hormones, they are typically produced locally and act in an autocrine or paracrine fashion. **2. Analysis of Incorrect Options:** * **Option B (Protein targets):** Cytokines do not act on "protein targets" in a general sense; they bind specifically to **high-affinity cell surface receptors**. This binding triggers an intracellular signaling cascade (most commonly the JAK-STAT pathway). * **Option C (Intrinsic enzymatic reactions):** Cytokines themselves do not possess intrinsic enzymatic activity. They function as ligands. While their receptors may activate enzymes (like Janus Kinases), the cytokine molecule is not an enzyme. * **Option D (Chemotaxis):** While a specific sub-family of cytokines called **chemokines** (e.g., IL-8) is involved in chemotaxis, the question asks what is true for cytokines *in general*. Not all cytokines are chemotactic; however, **all** cytokines are polypeptides. Therefore, Option A is the more fundamental biochemical truth. **3. High-Yield Clinical Pearls for NEET-PG:** * **Pleiotropy:** One cytokine having multiple effects on different cell types (e.g., IL-4 acting on B-cells, T-cells, and mast cells). * **Redundancy:** Multiple cytokines exerting the same effect (e.g., IL-2, IL-4, and IL-5 all trigger B-cell proliferation). * **Major Signaling Pathway:** Most cytokine receptors signal via the **JAK-STAT pathway**. * **Key Cytokines to Remember:** * **IL-1:** Endogenous pyrogen (causes fever). * **IL-8:** Major chemotactic factor for neutrophils ("Clean up on aisle 8"). * **TNF-α:** Mediator of septic shock and cachexia.

Question 457: What is common between B and T cells?

A. Origin from the same cell lineage (Correct Answer)
B. Site of differentiation
C. Antigenic marker
D. Involvement in both humoral and cellular immunity

Explanation: ### Explanation **1. Why Option A is Correct:** Both B and T lymphocytes originate from the **Common Lymphoid Progenitor (CLP)** cell, which is derived from **Hematopoietic Stem Cells (HSCs)** in the bone marrow. This shared lineage is the fundamental starting point for all adaptive immune cells. **2. Why the Other Options are Incorrect:** * **Option B (Site of Differentiation):** This is a key difference. **B cells** differentiate and mature in the **Bone marrow** (and fetal liver), whereas **T cells** migrate to and mature in the **Thymus**. * **Option C (Antigenic Marker):** They express distinct surface markers (Cluster of Differentiation). **B cells** are identified by **CD19, CD20, and CD21**, while **T cells** are identified by **CD3** (universal T-cell marker), CD4 (Helper), or CD8 (Cytotoxic). * **Option D (Involvement in Immunity):** While they cooperate, they have distinct roles. **B cells** are the primary mediators of **Humoral Immunity** (antibody production). **T cells** are the primary mediators of **Cell-Mediated Immunity**. **High-Yield Clinical Pearls for NEET-PG:** * **Null Cells:** Lymphocytes that lack both B and T cell markers are typically **Natural Killer (NK) cells**. * **Primary Lymphoid Organs:** Bone marrow and Thymus (where cells are "educated"). * **Secondary Lymphoid Organs:** Lymph nodes, Spleen, and MALT (where cells "meet" antigens). * **Memory:** Both B and T cells have the capacity for immunological memory, which is the basis for vaccination. * **DiGeorge Syndrome:** A classic exam topic where a failure of the 3rd and 4th pharyngeal pouches leads to thymic aplasia, resulting in a profound deficiency of T cells, while B cells remain intact.

Question 458: What is the most common immunoglobulin secreted by mother in milk and colostrum?

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

Explanation: **Explanation:** The correct answer is **IgA**. **1. Why IgA is correct:** Immunoglobulin A (IgA) is the predominant antibody found in all body secretions, including breast milk, colostrum, saliva, tears, and respiratory/gastrointestinal tracts. In milk and colostrum, it exists primarily as **Secretory IgA (sIgA)**, a dimer held together by a J-chain and protected from proteolytic enzymes by a **secretory component**. Its primary role is to provide **neonatal passive immunity**, protecting the infant's mucosal surfaces against enteric and respiratory pathogens before the infant's own immune system is fully functional. **2. Why the other options are incorrect:** * **IgG:** While IgG is the most abundant antibody in the *serum* and the only one that crosses the **placenta** to provide prenatal immunity, it is present in much lower concentrations in breast milk compared to IgA. * **IgE:** This antibody is primarily involved in type I hypersensitivity (allergic) reactions and defense against helminthic parasites. It is found in trace amounts in secretions. * **IgD:** This is mainly found on the surface of B-lymphocytes where it acts as an antigen receptor; it has no significant role in breast milk or passive immunity. **3. High-Yield Clinical Pearls for NEET-PG:** * **Colostrum vs. Milk:** Colostrum (the first milk) contains significantly higher concentrations of IgA than mature milk. * **Structure:** Remember that IgA is a **monomer in serum** but a **dimer in secretions**. * **MALT:** The IgA in milk is produced by plasma cells in the mammary glands that have migrated from the mother's gut-associated lymphoid tissue (GALT), a process known as the entero-mammary pathway. * **Most Common Deficiency:** Selective IgA deficiency is the most common primary immunodeficiency.

Question 459: Increased level of IgE is seen in which of the following conditions?

A. Atopy (Correct Answer)
B. Lepra reaction
C. Cutaneous Tuberculosis
D. Lupus vulgaris

Explanation: **Explanation:** **Correct Answer: A. Atopy** Immunoglobulin E (IgE) is the primary mediator of **Type I Hypersensitivity reactions**. In atopic individuals, there is a genetic predisposition to produce high levels of IgE in response to common environmental allergens. This process is driven by **Th2 cells**, which secrete IL-4 and IL-13, stimulating B-cells to undergo class-switching to IgE. The IgE then binds to high-affinity receptors (FcεRI) on mast cells and basophils, leading to degranulation upon re-exposure to the allergen. **Analysis of Incorrect Options:** * **B. Lepra reaction:** Type 1 lepra reactions are Type IV hypersensitivity (cell-mediated), while Type 2 lepra reactions (Erythema Nodosum Leprosum) are Type III hypersensitivity (immune-complex mediated). Neither is characterized by primary IgE elevation. * **C & D. Cutaneous Tuberculosis / Lupus vulgaris:** Lupus vulgaris is a common form of cutaneous TB. These represent a **Type IV (Delayed-type) hypersensitivity** response to *Mycobacterium tuberculosis*, involving T-lymphocytes and macrophages (granuloma formation), not IgE. **High-Yield Clinical Pearls for NEET-PG:** * **Job Syndrome (Hyper-IgE Syndrome):** Characterized by the triad of high IgE, recurrent "cold" staphylococcal abscesses, and coarse facial features (STAT3 mutation). * **Parasitic Infections:** IgE is also significantly elevated in helminthic infections (e.g., Ascariasis, Strongyloidiasis) to facilitate eosinophil-mediated killing. * **Prausnitz-Küstner (PK) Reaction:** An older method used to demonstrate IgE-mediated passive cutaneous anaphylaxis. * **Multiple Myeloma:** IgE myeloma is the rarest subtype of plasma cell dyscrasia.

Question 460: What is the central component of the complement system?

A. C3a
B. C3b
C. C4
D. C5 (Correct Answer)

Explanation: **Explanation:** The complement system is a biochemical cascade of the innate immune system. **C5** is considered the central component because it serves as the critical bridge between the activation pathways (Classical, Alternative, and Lectin) and the formation of the **Membrane Attack Complex (MAC)**. The cleavage of C5 by C5-convertase into C5a and C5b marks the final enzymatic step of the cascade. Once C5b is formed, it initiates the non-enzymatic assembly of C6, C7, C8, and C9 to form the MAC (C5b-9), which leads to cell lysis. **Analysis of Options:** * **C3a:** This is an anaphylatoxin released during C3 cleavage. While it mediates inflammation and chemotaxis, it is a byproduct rather than the central anchor for terminal pathway execution. * **C3b:** Often confused as the "central" molecule because it is the most abundant and acts as a potent opsonin. However, in the context of the entire cascade's progression toward cell death, C5 is the functional pivot. * **C4:** This is an early component of the Classical and Lectin pathways. It is involved in the formation of C3-convertase but does not participate in the Alternative pathway or the terminal MAC formation. **NEET-PG High-Yield Pearls:** * **Most abundant complement:** C3. * **Most potent anaphylatoxin:** C5a (C5a > C3a > C4a). * **Potent Opsonin:** C3b (facilitates phagocytosis via CR1 receptors). * **MAC Components:** C5b, C6, C7, C8, C9. * **Clinical Correlation:** Deficiency of late complement components (C5-C9) predisposes individuals to recurrent **Neisseria** infections.

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Complement System

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Hypersensitivity Reactions

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Immunology — MCQs

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