Immunology — MCQs

A patient presents with cerebellar problems and spider angiomas, diagnosed with ataxia-telangiectasia, a combined T-cell and B-cell deficiency. In addition to a defect in DNA repair enzymes, which immunoglobulin is the primary antibody found in saliva, tears, intestinal, and genital secretions and is also deficient in this condition?

Q878Easy

Cryoglobulins are present in the blood in which of the following clinical scenarios?

Q879Easy

Serum sickness occurs after:

Q880Easy

Which of the following cells do not act as antigen-presenting cells?

Immunology Indian Medical PG Practice Questions and MCQs

Question 871: Which of the following conditions is not due to complement deficiency?

A. Systemic Lupus Erythematosus (SLE)
B. Paroxysmal Nocturnal Hemoglobinuria (PNH) (Correct Answer)
C. Glomerulonephritis
D. Neisseria infection

Explanation: **Explanation** The correct answer is **B. Paroxysmal Nocturnal Hemoglobinuria (PNH)**. The key to this question lies in distinguishing between a **deficiency of complement proteins** and a **deficiency of complement regulatory proteins.** 1. **Why PNH is the correct answer:** PNH is not caused by a deficiency of complement proteins themselves. Instead, it is an acquired clonal stem cell disorder caused by a mutation in the **PIGA gene**. This leads to a deficiency of **GPI-anchored proteins**, specifically **CD55 (DAF)** and **CD59 (MIRL)**. These are regulatory proteins that normally protect RBCs from complement-mediated lysis. In PNH, the complement system is intact, but the RBCs lack the "shield" to stop it from attacking them. 2. **Why the other options are incorrect:** * **SLE (Option A):** Deficiencies of early classical pathway components (**C1q, C1r, C1s, C4, and C2**) are strongly associated with SLE-like syndromes because they are essential for the clearance of immune complexes. * **Glomerulonephritis (Option C):** Deficiencies in **C3** or regulatory factors like **Factor H** lead to uncontrolled complement activation and the deposition of immune complexes in the kidney, causing glomerulonephritis. * **Neisseria infection (Option D):** Deficiencies in the late components (**C5–C9**), which form the **Membrane Attack Complex (MAC)**, specifically predispose individuals to recurrent disseminated infections by *Neisseria meningitidis* and *Neisseria gonorrhoeae*. **High-Yield Clinical Pearls for NEET-PG:** * **C2 deficiency:** The most common complement deficiency in humans. * **C3 deficiency:** The most severe; presents with recurrent pyogenic infections (encapsulated bacteria). * **CH50 Assay:** Used to screen for classical pathway deficiencies. * **PNH Diagnosis:** Gold standard is **Flow Cytometry** showing absence of CD55/CD59.

Question 872: Which skin test is based on a neutralization reaction?

A. Casoni test
B. Lepromin test
C. Tuberculin test
D. Schick test (Correct Answer)

Explanation: ### Explanation The **Schick test** is a classic example of an **in vivo neutralization reaction** used to determine immunity against *Corynebacterium diphtheriae*. **1. Why Schick Test is Correct:** The test involves intradermal injection of a sub-lethal dose of **Diphtheria toxin**. * **If the person is immune:** Pre-existing circulating antitoxins (antibodies) neutralize the toxin, resulting in **no reaction** (Negative Schick test). * **If the person is susceptible:** The toxin is not neutralized, causing local inflammation and necrosis (Positive Schick test). Thus, the reaction directly measures the presence of neutralizing antibodies. **2. Why Other Options are Incorrect:** * **Casoni test (Option A):** An immediate **Type I Hypersensitivity** skin test used for diagnosing Hydatid disease (*Echinococcus granulosus*). It relies on IgE-mediated mast cell degranulation. * **Lepromin test (Option B):** A **Type IV (Delayed) Hypersensitivity** reaction used to classify Leprosy and assess the patient's cell-mediated immunity (CMI), not for diagnosis. * **Tuberculin test (Option C):** Also known as the Mantoux test, it is a classic **Type IV Hypersensitivity** reaction. It indicates prior exposure to *M. tuberculosis* and relies on sensitized T-lymphocytes. **3. High-Yield Clinical Pearls for NEET-PG:** * **Dick Test:** Another neutralization-based skin test used to identify susceptibility to Scarlet Fever (Streptococcal erythrogenic toxin). * **Schultz-Charlton Reaction:** A neutralization test where antitoxin is injected into a rash to see if it blanches (diagnostic for Scarlet Fever). * **Type IV Hypersensitivity Examples:** Tuberculin, Lepromin, Histoplasmin, and Frei tests. * **Control:** In the Schick test, the opposite arm is injected with **heat-inactivated toxin** to rule out pseudo-reactions (hypersensitivity to bacterial proteins).

Question 873: Which of the following conditions requires a large antigen-antibody reaction to cause?

A. Serum sickness
B. Autoimmune hemolytic anemia (Correct Answer)
C. Urticaria
D. Anaphylactic reaction

Explanation: **Explanation:** The question focuses on the quantitative requirement of antigen-antibody interactions across different hypersensitivity reactions. **Why Option B is Correct:** **Autoimmune Hemolytic Anemia (AIHA)** is a **Type II Hypersensitivity** reaction. In Type II reactions, antibodies (IgG or IgM) are directed against antigens on specific cell surfaces (the RBC membrane in this case). Because the antigen is a structural component of a cell, a **large amount of antigen-antibody reaction** is required to cause significant clinical hemolysis. The density of antigens on the cell surface and the subsequent binding of numerous antibodies are necessary to trigger effective complement activation or opsonization by splenic macrophages. **Why Other Options are Incorrect:** * **A. Serum Sickness:** This is a **Type III Hypersensitivity** reaction. It is characterized by the formation of small, soluble immune complexes that circulate and deposit in tissues. It is triggered by an **excess of antigen**, not necessarily a "large" total reaction volume. * **C & D. Urticaria and Anaphylaxis:** These are **Type I Hypersensitivity** reactions mediated by IgE. These reactions are notorious for being triggered by **minute quantities** of an antigen (allergen). A single molecule of allergen can cross-link IgE on a mast cell, leading to massive degranulation; thus, they do not require a large reaction to manifest symptoms. **NEET-PG High-Yield Pearls:** * **Type I:** IgE mediated, "Immediate," requires minimal antigen (e.g., Penicillin anaphylaxis). * **Type II:** Cytotoxic, antibody-mediated (e.g., AIHA, Goodpasture syndrome, Myasthenia Gravis). * **Type III:** Immune-complex mediated, "Ag-Ab complexes" (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type IV:** T-cell mediated, "Delayed" (e.g., Mantoux test, Contact dermatitis).

Question 874: What is the maximum serum concentration among the following human immunoglobulins?

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

Explanation: ### Explanation The correct answer is **IgG**. Immunoglobulins (antibodies) are classified into five types based on their heavy chains. Their serum concentrations vary significantly, and remembering the mnemonic **"GAMED"** helps recall their order of abundance from highest to lowest. **1. Why IgG is Correct:** IgG is the most abundant class of immunoglobulin in human serum, accounting for approximately **75% to 80%** of the total pool. It has a concentration of about 8–16 mg/mL. Its high concentration is due to its long half-life (approx. 23 days) and its role as the primary antibody in the secondary immune response. **2. Why the Other Options are Incorrect:** * **IgA (Option B):** It is the second most abundant (~10–15%). While it is the predominant antibody in **secretions** (tears, saliva, colostrum), its serum concentration is lower than IgG. * **IgM (Option C):** It accounts for about 5–10% of serum antibodies. It is the largest (pentamer) and the first to appear in a primary immune response, but it does not reach the high serum levels of IgG. * **IgD (Option D):** It is found in trace amounts (<1%) in the serum and primarily acts as a B-cell receptor. * **IgE (Not listed):** Present in the lowest concentration, primarily involved in Type I hypersensitivity and parasitic infections. **Clinical Pearls for NEET-PG:** * **IgG:** The only immunoglobulin that can **cross the placenta**, providing passive immunity to the fetus. * **IgM:** The best at **complement fixation** (classical pathway) and the first antibody synthesized by the fetus. * **IgA:** Exists as a monomer in serum but as a **dimer** (with a J-chain and secretory component) in secretions. * **Half-life:** IgG has the longest half-life (23 days), except for the IgG3 subclass.

Question 875: Which of the following is involved in innate immunity?

A. T-cells
B. B-cells
C. Macrophages (Correct Answer)
D. Antibodies

Explanation: **Explanation:** Immunity is broadly classified into **Innate (Non-specific)** and **Acquired (Adaptive/Specific)** immunity. **Why Macrophages are the Correct Answer:** Macrophages are key cellular components of the **Innate Immune System**. They act as the first line of defense through **phagocytosis**. They possess Pattern Recognition Receptors (PRRs), such as Toll-Like Receptors (TLRs), which recognize conserved microbial structures (PAMPs) without prior exposure to the pathogen. Unlike the adaptive system, innate immunity is present from birth, lacks memory, and responds immediately. **Analysis of Incorrect Options:** * **A. T-cells:** These are the primary mediators of **Cell-Mediated Immunity (CMI)**, a branch of the Acquired Immune System. They require antigen presentation and undergo clonal expansion. * **B. B-cells:** These are the mediators of **Humoral Immunity**, also a part of the Acquired Immune System. They differentiate into plasma cells to produce specific antibodies. * **D. Antibodies:** Also known as Immunoglobulins, these are products of B-cells. They represent the **specific effector molecules** of acquired immunity, designed to target unique antigens. **NEET-PG High-Yield Pearls:** * **Components of Innate Immunity:** Physical barriers (Skin/Mucosa), Chemical barriers (Gastric acid/Lysozyme), Cells (Neutrophils, Macrophages, NK cells, Dendritic cells), and the Complement system (Alternative and Lectin pathways). * **Bridge between systems:** Macrophages and Dendritic cells are "Antigen Presenting Cells" (APCs); they process antigens from the innate phase to activate the adaptive phase (T-cells). * **NK Cells:** Important NEET-PG fact—NK cells are **lymphocytes** but function as part of **innate** immunity.

Question 876: Which immunoglobulin activates complement via the alternative pathway?

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

Explanation: **Explanation:** The activation of the complement system occurs via three main pathways: Classical, Alternative, and Lectin. **Why IgA is correct:** While the Classical pathway is triggered by antigen-antibody complexes involving IgG or IgM, the **Alternative pathway** is primarily antibody-independent (triggered by microbial surfaces, endotoxins, or cobra venom). However, among the immunoglobulins, **aggregated IgA** (specifically IgA1 and IgA2) is unique because it can trigger the alternative pathway. It bypasses C1, C4, and C2, acting directly on C3. **Analysis of Incorrect Options:** * **IgM:** This is the most potent activator of the **Classical pathway** due to its pentameric structure, which provides multiple binding sites for the C1q component. * **IgG:** This activates the **Classical pathway**. Among its subclasses, IgG3 is the most effective, followed by IgG1 and IgG2 (IgG4 does not activate complement). * **IgE:** This immunoglobulin is primarily involved in Type I hypersensitivity reactions and helminthic immunity; it does not play a significant role in complement activation. **High-Yield Clinical Pearls for NEET-PG:** * **Classical Pathway:** Triggered by **IgM** (most potent) and **IgG** (1, 2, and 3). Remember: "GM makes it Classic." * **Alternative Pathway:** Triggered by **IgA**, IgD (rarely), endotoxins, and the "Factor" proteins (B, D, and Properdin). * **C3:** This is the common point where all three pathways converge. * **IgA Deficiency:** The most common primary immunodeficiency; patients may have anaphylactic reactions when receiving blood transfusions containing IgA.

Question 877: A patient presents with cerebellar problems and spider angiomas, diagnosed with ataxia-telangiectasia, a combined T-cell and B-cell deficiency. In addition to a defect in DNA repair enzymes, which immunoglobulin is the primary antibody found in saliva, tears, intestinal, and genital secretions and is also deficient in this condition?

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

Explanation: ### Explanation **Correct Option: B. IgA** **Concept:** Ataxia-telangiectasia (AT) is an autosomal recessive multisystem disorder caused by a mutation in the **ATM gene**, which is responsible for repairing double-stranded DNA breaks. This defect leads to genomic instability, affecting lymphocyte development. While AT is a combined immunodeficiency, the most characteristic and common humoral defect is a **selective deficiency of IgA**. IgA is the primary mediator of **mucosal immunity**. It exists as a monomer in the serum but forms a **dimer** (connected by a J-chain) in secretions. It is the predominant antibody found in "external" fluids such as **saliva, tears, colostrum, bronchial, intestinal, and genitourinary secretions**, where it prevents the attachment of pathogens to epithelial surfaces. **Why other options are incorrect:** * **IgG:** This is the most abundant antibody in the **serum** and the only one that crosses the placenta. While IgG subclasses (like IgG2) can be low in AT, it is not the primary secretory antibody. * **IgM:** This is the first antibody produced in a primary immune response and exists as a **pentamer**. It is primarily intravascular and not the dominant secretory immunoglobulin. * **IgD:** Found mainly on the surface of B-cells as an antigen receptor; its systemic secretory function is negligible. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad of AT:** Cerebellar ataxia (staggering gait), Telangiectasia (spider angiomas, especially in the conjunctiva), and Recurrent sinopulmonary infections. * **Laboratory Markers:** Elevated **Alpha-fetoprotein (AFP)** levels (after age 1) are a highly specific diagnostic clue for AT. * **Risk:** Patients have a significantly increased risk of malignancies, particularly **Lymphomas and Leukemias**, due to DNA repair failure. * **Radiology:** Look for **Cerebellar atrophy** on MRI.

Question 878: Cryoglobulins are present in the blood in which of the following clinical scenarios?

A. Macroglobulinaemia
B. Systemic Lupus Erythematosus (SLE)
C. Myeloma
D. All the above (Correct Answer)

Explanation: **Explanation:** Cryoglobulins are abnormal immunoglobulins (antibodies) that reversibly precipitate at low temperatures (below 37°C) and dissolve upon rewarming. They are categorized into three types based on the Brouet classification, and their presence is associated with various lymphoproliferative and autoimmune disorders. * **Macroglobulinemia (Waldenström’s):** This condition involves a monoclonal IgM spike. These large IgM molecules often act as **Type I cryoglobulins** (monoclonal), leading to hyperviscosity and vascular occlusion. * **Systemic Lupus Erythematosus (SLE):** SLE is a classic example of a condition causing **Type III cryoglobulinemia** (mixed polyclonal). Here, immune complexes (IgG and anti-IgG) circulate in the blood, often seen in chronic inflammatory or autoimmune states. * **Myeloma (Multiple Myeloma):** Plasma cell dyscrasias like Multiple Myeloma produce monoclonal IgG or IgA. These can function as **Type I cryoglobulins**, especially when protein levels are significantly elevated. Since cryoglobulins can be monoclonal (Type I) or mixed (Type II/III), they are found across the spectrum of both neoplastic B-cell disorders and systemic autoimmune diseases. Therefore, **All the above** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Association:** Hepatitis C virus (HCV) is the most common cause of Type II (mixed monoclonal/polyclonal) cryoglobulinemia. * **Meltzer’s Triad:** The classic clinical presentation includes **purpura, arthralgia, and weakness**. * **Lab Diagnosis:** Blood must be collected in a pre-warmed syringe and kept at 37°C until clotting to prevent premature precipitation before laboratory analysis. * **Complement Levels:** Cryoglobulinemia typically presents with **low C4 levels** but often normal C3 levels.

Question 879: Serum sickness occurs after:

A. Injection with foreign serum (Correct Answer)
B. Injection with own serum
C. Injection with normal saline
D. All of the above

Explanation: **Explanation:** Serum sickness is a classic example of a **Type III Hypersensitivity reaction** (Immune-complex mediated). It occurs when a large amount of foreign antigen is introduced into the body, leading to the formation of soluble antigen-antibody complexes that deposit in small blood vessels, activating the complement system and causing tissue damage. * **Why Option A is correct:** Serum sickness was historically described after the administration of horse serum (antitoxin) for diphtheria or tetanus. When **foreign serum** (containing foreign proteins) is injected, the body recognizes these proteins as antigens and produces antibodies (usually IgG). These antibodies bind to the circulating foreign proteins, forming complexes that deposit in joints, kidneys, and vessels, typically manifesting 7–14 days after exposure. * **Why Options B and C are incorrect:** **Own serum** (autologous) and **Normal saline** (isotonic salt solution) are not recognized as foreign by the immune system. They lack the "non-self" immunogenic proteins required to trigger an antibody response and subsequent immune-complex formation. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Fever, Rash (urticaria), and Arthralgia. * **Mechanism:** It is a **systemic** Type III hypersensitivity (unlike the Arthus reaction, which is localized). * **Complement Levels:** Characterized by **low serum complement levels** (C3 and C4) due to massive consumption during the reaction. * **Modern Triggers:** Today, it is more commonly caused by non-protein drugs like **Penicillin**, sulfonamides, or monoclonal antibodies (e.g., Rituximab).

Question 880: Which of the following cells do not act as antigen-presenting cells?

A. T-cells (Correct Answer)
B. B-cells
C. Macrophages
D. Osteoclasts

Explanation: **Explanation:** Antigen-presenting cells (APCs) are specialized immune cells that capture, process, and display antigens on their surface via **MHC Class II** molecules to activate T-lymphocytes. **1. Why T-cells are the correct answer:** T-cells are the **recipients** of the antigen presentation, not the presenters. They possess T-cell receptors (TCRs) that recognize antigens displayed by APCs. While T-cells are central to the adaptive immune response, they lack the MHC Class II machinery required to function as professional APCs. **2. Analysis of other options:** * **B-cells:** These are "Professional APCs." They internalize antigens via surface immunoglobulins and present them to Helper T-cells to receive signals for antibody production. * **Macrophages:** These are classic Professional APCs. They phagocytose pathogens and present processed peptides to T-cells to initiate cell-mediated immunity. * **Osteoclasts:** These are "Non-professional APCs." Derived from the monocyte-macrophage lineage, osteoclasts express MHC Class II and can present antigens to T-cells, particularly in the context of inflammatory bone diseases. **High-Yield NEET-PG Pearls:** * **Professional APCs:** Dendritic cells (most potent), Macrophages, and B-cells. * **Dendritic Cells:** Specifically, **Langerhans cells** in the skin are the most efficient APCs for priming naive T-cells. * **MHC Restriction:** APCs present to **CD4+ T-cells** via MHC Class II, whereas all nucleated cells can present endogenous antigens to **CD8+ T-cells** via MHC Class I. * **Follicular Dendritic Cells (FDCs):** Unlike regular DCs, FDCs in lymph nodes trap antigens via complement receptors and do not use MHC Class II.

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Complement System

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Cytokines and Chemokines

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Immunology — MCQs

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