Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 901: A 1-year-old child presents with cyanosis during breastfeeding, which resolves upon squatting. A cleft palate is noted on examination, and laboratory tests reveal hypocalcemia. Which of the following abnormalities are expected to be seen in the lymphoid organs?

A. Decreased size of the periaeriolar lymphoid sheath of the spleen (Correct Answer)
B. Increased size of splenic follicles
C. Increased size of paracortical areas of lymph nodes
D. Decreased size of germinal centers of lymph nodes

Explanation: ### **Explanation** **Clinical Diagnosis: DiGeorge Syndrome** The clinical triad of **cyanotic heart disease** (suggestive of Tetralogy of Fallot, indicated by "squatting" to relieve cyanosis), **cleft palate**, and **hypocalcemia** (due to hypoparathyroidism) points to **DiGeorge Syndrome**. This condition results from a microdeletion on chromosome **22q11.2**, leading to the failure of the **3rd and 4th pharyngeal pouches** to develop. #### **1. Why the Correct Answer is Right** In DiGeorge Syndrome, there is **thymic aplasia or hypoplasia**, resulting in a profound deficiency of **T-lymphocytes**. In lymphoid organs, T-cells specifically populate "T-cell dependent zones." * **Spleen:** The **Periarteriolar Lymphoid Sheath (PALS)** is the T-cell zone. Due to T-cell deficiency, the PALS will be depleted or decreased in size. * **Lymph Nodes:** The **paracortex** is the T-cell zone and would also be depleted. #### **2. Why the Incorrect Options are Wrong** * **B & D (Splenic follicles/Germinal centers):** These are **B-cell dependent areas**. In DiGeorge syndrome, B-cell numbers and the humoral response are generally preserved initially; therefore, these areas are not typically decreased in size. * **C (Increased paracortical areas):** The paracortex is a T-cell zone. In T-cell deficiency, this area would be **decreased/depleted**, not increased. #### **3. High-Yield Clinical Pearls for NEET-PG** * **CATCH-22 Mnemonic:** **C**ardiac defects (Truncus arteriosus/ToF), **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia (due to parathyroid aplasia), **22**q11 deletion. * **Immunology:** Patients have recurrent viral, fungal, and protozoal infections due to defective cell-mediated immunity. * **Radiology:** Look for the absence of a **"Thymic Shadow"** on a pediatric chest X-ray. * **Histology:** T-cell zones (Paracortex of lymph nodes and PALS of spleen) are the specific sites of pathology in T-cell immunodeficiencies.

Question 902: Helper T-cells are primarily involved in which aspect of the immune response?

A. Cell-mediated immunity (Correct Answer)
B. Killing virus-infected cells
C. Killing tumor cells
D. Type II hypersensitivity reactions

Explanation: **Explanation:** **1. Why Option A is Correct:** Helper T-cells (CD4+ T-cells) are the central orchestrators of **Cell-Mediated Immunity (CMI)**. Upon recognizing antigens presented by MHC Class II molecules, they differentiate into subsets (like Th1 and Th2). Th1 cells specifically secrete cytokines such as **Interferon-gamma (IFN-γ)** and **IL-2**, which activate macrophages, natural killer cells, and cytotoxic T-lymphocytes. This process is essential for eliminating intracellular pathogens (e.g., *M. tuberculosis*) and is the hallmark of the CMI response. **2. Why Other Options are Incorrect:** * **Options B & C:** Killing virus-infected and tumor cells is the primary function of **Cytotoxic T-cells (CD8+)** and **Natural Killer (NK) cells**. While Helper T-cells "help" activate these cells, they do not perform the direct "killing" (perforin/granzyme-mediated apoptosis) themselves. * **Option D:** Type II Hypersensitivity is **antibody-mediated** (IgG/IgM), involving complement activation or ADCC. Helper T-cells are more directly associated with **Type IV (Delayed-type) Hypersensitivity**. **NEET-PG High-Yield Pearls:** * **CD4:CD8 Ratio:** The normal ratio in peripheral blood is approximately **2:1**. This ratio is characteristically reversed (<1) in HIV/AIDS. * **Th1 vs. Th2:** Th1 cells drive CMI (via IL-2, IFN-γ); Th2 cells drive Humoral Immunity/allergy (via IL-4, IL-5, IL-13). * **MHC Restriction:** Remember the **"Rule of 8"**: CD4 x MHC II = 8; CD8 x MHC I = 8. Helper T-cells only recognize antigens on MHC II.

Question 903: Which of the following complications is currently the major limitation to the long-term success of cardiac transplantation?

A. Allograft rejection
B. Graft arteriosclerosis (Correct Answer)
C. Graft atherosclerosis
D. Opportunistic infections

Explanation: **Explanation:** The correct answer is **Graft arteriosclerosis** (also known as Cardiac Allograft Vasculopathy - CAV). **Why it is correct:** While acute rejection was historically the primary concern, modern immunosuppressive therapy (like Cyclosporine and Tacrolimus) has significantly improved short-term survival. Currently, the major limitation to **long-term** success (beyond 1 year) is **Graft Arteriosclerosis**. This is a form of **chronic rejection** characterized by concentric, diffuse intimal thickening of the coronary arteries. Unlike typical atherosclerosis, it affects the entire length of the vessel and is primarily mediated by a T-cell-driven chronic inflammatory response against the graft endothelium. **Why other options are incorrect:** * **A. Allograft rejection:** Acute cellular or humoral rejection is the leading cause of graft failure in the **first year**, but it is no longer the primary long-term limitation due to effective immunosuppression. * **C. Graft atherosclerosis:** This term is technically incorrect in this context. Traditional atherosclerosis is focal and eccentric, whereas graft arteriosclerosis is diffuse and concentric. * **D. Opportunistic infections:** These are significant causes of morbidity and mortality in the **early post-transplant period** (especially months 1–6) due to peak immunosuppression, but they are not the primary cause of long-term graft failure. **High-Yield Clinical Pearls for NEET-PG:** * **Chronic Rejection Mechanism:** Type IV Hypersensitivity (T-cell mediated) leading to vascular smooth muscle proliferation. * **Clinical Presentation:** Patients with graft arteriosclerosis often do not experience angina because the transplanted heart is **denervated**. They may present directly with heart failure or sudden cardiac death. * **Timeline:** Acute rejection (<6 months); Chronic rejection/Graft arteriosclerosis (>6 months to years).

Question 904: Which immunoglobulin is primarily secreted in bronchial secretions?

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

Explanation: **Explanation:** The correct answer is **IgA**. **Why IgA is correct:** IgA is the primary immunoglobulin associated with mucosal immunity. In the body, it exists in two forms: monomeric (in serum) and dimeric (in secretions). **Secretory IgA (sIgA)** is specifically adapted to survive in harsh external environments due to the presence of a **J-chain** (which holds the dimer together) and a **secretory component** (which protects the antibody from proteolytic enzymes). It is the predominant antibody found in bronchial secretions, saliva, tears, colostrum, and gastrointestinal secretions, acting as the first line of defense against inhaled or ingested pathogens by preventing microbial adherence to mucosal surfaces. **Why other options are incorrect:** * **IgE:** Primarily involved in Type I hypersensitivity reactions (allergy/anaphylaxis) and host defense against helminthic parasitic infections. While present in the respiratory tract during asthma, it is not the primary constitutive secretory antibody. * **IgM:** The first antibody produced in a primary immune response. It is a pentamer and is too large to be the primary secretory antibody, though it can be secreted in small amounts if IgA is deficient. * **IgG:** The most abundant immunoglobulin in serum and the only one that crosses the placenta. It provides systemic immunity rather than mucosal surface protection. **High-Yield Clinical Pearls for NEET-PG:** * **Selective IgA Deficiency:** The most common primary immunodeficiency; patients often present with recurrent sinopulmonary and GI infections. * **Secretory Component:** It is derived from the poly-Ig receptor on the surface of epithelial cells, not from the plasma cells. * **Milk:** IgA provides passive immunity to the newborn via breast milk (colostrum).

Question 905: A positive Schick test indicates that a person is?

A. Immune to diphtheria
B. Hypersensitive to diphtheria
C. Susceptible to diphtheria (Correct Answer)
D. Carrier of diphtheria

Explanation: ### Explanation The **Schick test** is a classic skin test used to determine the immune status of an individual against *Corynebacterium diphtheriae*. It works on the principle of **toxin-antitoxin neutralization**. **Why Option C is Correct:** A person is considered **susceptible** if they lack circulating antitoxin (antibodies) against the diphtheria toxin. In the test, 0.1 ml of purified diphtheria toxin is injected intradermally into one forearm (test) and inactivated toxin into the other (control). If the person lacks immunity, the toxin remains active and causes a localized inflammatory reaction (erythema and swelling) at the injection site within 4–7 days. This is a **Positive Result**, indicating susceptibility. **Why Other Options are Incorrect:** * **Option A:** If a person is **immune**, their circulating antitoxin neutralizes the injected toxin, resulting in no skin reaction (Negative Result). * **Option B:** Hypersensitivity is detected by a **Pseudo-reaction**, where both the test and control arms show a reaction that disappears rapidly (within 48 hours). This indicates an allergy to the bacterial proteins, not susceptibility to the toxin. * **Option D:** A carrier state is identified through throat or nasal swabs and culture (e.g., on Löffler's serum slope), not by the Schick test, which only measures humoral immunity. ### NEET-PG High-Yield Pearls: * **Positive Reaction:** Erythema (10–50 mm) reaching peak at 4–7 days. Indicates **Susceptibility**. * **Negative Reaction:** No reaction on either arm. Indicates **Immunity**. * **Combined Reaction:** Both arms show reaction, but the test arm reaction is larger and lasts longer. Indicates both **Susceptibility and Hypersensitivity**. * **Current Status:** The Schick test is largely obsolete in clinical practice due to the widespread use of the DPT/Pentavalent vaccine, but it remains a frequent topic in competitive exams.

Question 906: Apart from T and B lymphocytes, what is the other major class of lymphocytes?

A. Macrophages
B. Astrocytes
C. NK cells (Correct Answer)
D. Langerhans cells

Explanation: **Explanation:** Lymphocytes are a subtype of white blood cells categorized into three major populations: **T cells, B cells, and Natural Killer (NK) cells.** While T and B cells are the mediators of adaptive immunity, NK cells are the primary lymphoid component of the **innate immune system.** **Why NK cells are the correct answer:** NK cells are large granular lymphocytes that do not express antigen-specific receptors (like TCR or BCR). Instead, they identify stressed, virally infected, or tumor cells through a "balance of signals" from activating and inhibitory receptors. Their hallmark is the ability to kill cells that have downregulated **MHC Class I** molecules (the "missing self" hypothesis). **Analysis of Incorrect Options:** * **Macrophages (A):** These are mononuclear phagocytes derived from **monocytes**, not lymphocytes. They function as professional antigen-presenting cells (APCs). * **Astrocytes (B):** These are non-immune **glial cells** of the Central Nervous System (CNS) responsible for maintaining the blood-brain barrier and providing structural support. * **Langerhans cells (D):** These are specialized **dendritic cells** found in the stratum spinosum of the epidermis. Like macrophages, they are myeloid in origin, not lymphoid. **High-Yield Facts for NEET-PG:** * **Surface Markers:** NK cells are typically identified as **CD3–, CD56+, and CD16+** (FcγRIII). * **Mechanism of Action:** They induce apoptosis via **perforins and granzymes** or through the Fas/FasL pathway. * **Cytokine Production:** They are a major source of **IFN-gamma**, which activates macrophages. * **Clinical Correlation:** Deficiency in NK cell function leads to increased susceptibility to viral infections (especially Herpesviruses) and certain malignancies.

Question 907: Which of the following features is not shared between T cells and B cells?

A. Positive selection during development (Correct Answer)
B. Class I MHC expression
C. Antigen-specific receptors
D. All of the above

Explanation: **Explanation:** The core difference in the development of T and B lymphocytes lies in their **selection processes** within primary lymphoid organs. **1. Why Option A is correct:** **Positive selection** is a process unique to **T cell development** in the thymus. It ensures that T cells can recognize self-MHC molecules; those that cannot bind are eliminated via apoptosis. **B cells do not undergo positive selection.** They only undergo **negative selection** in the bone marrow, where self-reactive B cells are eliminated or undergo receptor editing to ensure self-tolerance. **2. Why other options are incorrect:** * **Option B (Class I MHC expression):** All nucleated cells in the human body express MHC Class I molecules. Since both B cells and T cells are nucleated lymphocytes, they both express MHC Class I. (Note: B cells also express MHC Class II as they are professional antigen-presenting cells). * **Option C (Antigen-specific receptors):** Both cell types possess highly specific receptors generated by V(D)J recombination. B cells have **BCRs** (membrane-bound antibodies), and T cells have **TCRs**. Both are designed to recognize specific antigens. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Maturation:** B cells mature in the **B**one marrow; T cells mature in the **T**hymus. * **Negative Selection:** Occurs in **both** B and T cells to prevent autoimmunity (Central Tolerance). * **MHC Restriction:** T cells are "MHC restricted" (require MHC to see antigen), whereas B cells can recognize free, native antigens directly. * **Double Positive Stage:** Only T cells go through a CD4+ CD8+ stage during thymic maturation.

Question 908: Which of the following are examples of delayed type hypersensitivity reactions?

A. Arthus reaction
B. Bronchial asthma
C. Hemolytic anemia (Correct Answer)
D. Multiple sclerosis

Explanation: **Explanation** Hypersensitivity reactions are classified by the Gell and Coombs system into four types. **Delayed-type hypersensitivity (DTH)** is **Type IV**, which is cell-mediated (T-cells and macrophages) rather than antibody-mediated, typically occurring 48–72 hours after exposure. **Why the Correct Answer is Right:** * **Multiple Sclerosis (Option D):** This is a classic example of a Type IV hypersensitivity reaction. It involves T-cell-mediated destruction of the myelin sheath in the central nervous system. (Note: There appears to be a discrepancy in the provided key; while Hemolytic Anemia is marked, **Multiple Sclerosis** is the standard example of Type IV, whereas Hemolytic Anemia is Type II). **Analysis of Other Options:** * **A. Arthus Reaction:** This is a localized **Type III** hypersensitivity reaction. It involves the deposition of antigen-antibody (immune) complexes in tissue, leading to complement activation and neutrophil recruitment. * **B. Bronchial Asthma:** This is a **Type I** (Immediate) hypersensitivity reaction. It is mediated by IgE antibodies causing mast cell degranulation and the release of histamine and leukotrienes. * **C. Hemolytic Anemia:** This is a **Type II** (Cytotoxic) hypersensitivity reaction. It involves IgG or IgM antibodies binding to antigens on the surface of red blood cells, leading to their destruction via the complement system or phagocytosis. **NEET-PG High-Yield Pearls:** * **Type IV Examples (Mnemonic: 4 Ts):** **T**-cells, **T**ests (Mantoux/Patch test), **T**ransplant rejection (Chronic), and **T**errible skin conditions (Contact dermatitis). * **Type II vs. Type III:** Type II involves antibodies binding to **fixed** cell-surface antigens; Type III involves **soluble** circulating immune complexes. * **Granuloma formation:** This is the hallmark of persistent Type IV reactions (e.g., Tuberculosis, Sarcoidosis).

Question 909: What is true about superantigens?

A. They bind to the Vβ region of the T cell receptor.
B. They need to be processed before presentation.
C. They are presented by antigen-presenting cells to B cells.
D. They bind to the MHC class II molecule on antigen-presenting cells and the variable region of the T cell receptor. (Correct Answer)

Explanation: ### Explanation **Concept Overview:** Superantigens are potent immunostimulatory molecules (mostly bacterial toxins) that bypass the conventional rules of antigen presentation. Unlike conventional antigens, they do not require intracellular processing. Instead, they bind directly to the **external surface** of the **MHC class II molecule** on Antigen-Presenting Cells (APCs) and the **Variable region of the Beta chain (Vβ)** of the T-cell receptor (TCR). This results in a massive, non-specific activation of T-cells (up to 20%), leading to a "cytokine storm" (IL-1, IL-2, TNF-α, and IFN-γ). **Analysis of Options:** * **Option D (Correct):** Accurately describes the "bridge" formed by superantigens between the MHC II of the APC and the TCR, leading to polyclonal T-cell activation. * **Option A (Incorrect):** While they do bind to the Vβ region, this option is incomplete as it ignores the crucial interaction with the MHC class II molecule on the APC. * **Option B (Incorrect):** Conventional antigens are processed into peptides; superantigens are **not processed** and bind directly in their native form. * **Option C (Incorrect):** Superantigens are presented to **T-cells**, not B-cells. **High-Yield Clinical Pearls for NEET-PG:** 1. **Examples of Superantigens:** * *Staphylococcus aureus:* TSST-1 (Toxic Shock Syndrome Toxin), Exfoliative toxin (Scalded Skin Syndrome), and Enterotoxins (Food poisoning). * *Streptococcus pyogenes:* SpeA and SpeC (Erythrogenic toxins causing Scarlet fever/Toxic shock). 2. **Endogenous Superantigens:** Certain viral proteins integrated into the genome (e.g., Mouse Mammary Tumor Virus). 3. **Clinical Consequence:** The massive release of **TNF-α** is primarily responsible for the hypotension and shock seen in Toxic Shock Syndrome.

Question 910: Which immunoglobulin activates the classical complement pathway?

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

Explanation: **Explanation:** The classical complement pathway is initiated by the binding of the **C1 complex** (specifically the C1q subunit) to the **Fc portion** of an antibody that is already bound to an antigen. **Why IgM is the correct answer:** IgM is the most potent activator of the classical pathway. This is due to its **pentameric structure**. C1q requires binding to at least two Fc fragments simultaneously to become activated. Since a single molecule of pentameric IgM has five Fc portions in close proximity, it provides multiple binding sites, making it highly efficient at "fixing" complement. Even a single molecule of IgM bound to a red cell can initiate the cascade. **Analysis of incorrect options:** * **IgG (Option B):** While IgG (specifically IgG3, IgG1, and IgG2) can activate the classical pathway, it is significantly less efficient than IgM. Because IgG is a monomer, at least two IgG molecules must land side-by-side on an antigen surface to allow C1q to bridge them. * **IgA (Option A):** IgA does not activate the classical pathway. It can, however, activate the **Alternative pathway** (specifically in its aggregated form). * **IgD (Option D):** IgD is primarily found on the surface of B cells and does not play a significant role in complement activation. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Classical Pathway:** "**GM** makes **C**lassic cars" (Ig**G** and Ig**M** activate the **C**lassical pathway). * **Potency Order:** IgM > IgG3 > IgG1 > IgG2. (Note: IgG4 does *not* activate complement). * **Alternative Pathway Activators:** IgA, IgE, Endotoxins, and Cobra Venom Factor. * **Lectin Pathway:** Activated by Mannose-binding lectin (MBL) binding to carbohydrates on microbial surfaces; it does not require antibodies.

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Cells and Organs of Immune System

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Innate Immunity

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Adaptive Immunity

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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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Tumor Immunology

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Immunology — MCQs

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