Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 41: Which of the following is an example of an immune complex hypersensitivity reaction?

A. Atopic allergy
B. Serum sickness (Correct Answer)
C. Transfusion reaction
D. Contact dermatitis

Explanation: ### Explanation **Correct Answer: B. Serum sickness** **Serum sickness** is the classic clinical example of **Type III Hypersensitivity (Immune Complex-mediated)**. In this reaction, soluble antigens react with IgG or IgM antibodies to form **antigen-antibody complexes**. These complexes circulate and eventually deposit in various tissues (like blood vessel walls, synovial membranes, and renal glomeruli). Once deposited, they activate the **classical complement pathway**, leading to neutrophil recruitment, lysosomal enzyme release, and subsequent tissue damage (vasculitis, arthritis, and nephritis). **Analysis of Incorrect Options:** * **A. Atopic allergy:** This is a **Type I (Immediate)** hypersensitivity reaction. It is mediated by **IgE** antibodies binding to mast cells and basophils, leading to the release of histamine and other vasoactive amines upon re-exposure to an allergen. * **C. Transfusion reaction:** This is typically a **Type II (Cytotoxic)** hypersensitivity reaction. It involves **IgG or IgM** antibodies binding directly to antigens on the surface of cells (like donor RBCs), leading to cell lysis via complement activation or ADCC. * **D. Contact dermatitis:** This is a **Type IV (Delayed-type)** hypersensitivity reaction. It is **cell-mediated** (T-cells), not antibody-mediated, and typically occurs 48–72 hours after exposure to haptens like nickel or poison ivy. **High-Yield Clinical Pearls for NEET-PG:** * **Type III Mnemonic:** Remember **"S-A-P"** for Type III: **S**erum sickness, **A**rthus reaction, and **P**ost-streptococcal glomerulonephritis (PSGN). * **Serum Sickness vs. Arthus Reaction:** Serum sickness is **systemic** (generalized), whereas the Arthus reaction is a **localized** area of tissue necrosis (usually following a booster vaccine). * **Complement levels:** In Type III reactions, serum complement levels (C3, C4) are typically **decreased** due to massive consumption during the inflammatory process.

Question 42: Interleukin-2 (IL-2) activates Th1/CD4+ cells through which of the following mechanisms?

A. NK cells
B. Th cells
C. T memory cells
D. All the above (Correct Answer)

Explanation: **Explanation:** Interleukin-2 (IL-2), originally known as **T-cell Growth Factor**, is a cytokine primarily produced by CD4+ T-helper cells (specifically Th1 cells) following antigen stimulation. It acts via **autocrine and paracrine** signaling to drive the proliferation and differentiation of various immune cells. **Why "All the Above" is Correct:** IL-2 is a potent "pan-T cell" stimulator. Its primary functions include: * **Th cells (Option B):** IL-2 promotes the clonal expansion of T-helper cells (CD4+), particularly driving the Th1 response. * **T memory cells (Option C):** It is essential for the development and long-term maintenance of memory T cells, ensuring a rapid response upon re-exposure to an antigen. * **NK cells (Option A):** IL-2 enhances the cytolytic activity of Natural Killer (NK) cells and induces their proliferation. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **IL-2 Receptor (CD25):** The high-affinity IL-2 receptor is composed of three chains: $\alpha$ (CD25), $\beta$ (CD122), and $\gamma$ (CD132). CD25 is a classic marker for activated T cells and Regulatory T cells (Tregs). * **Treg Maintenance:** While IL-2 stimulates effector cells, it is also paradoxically crucial for the survival of **Tregs**, which prevent autoimmunity. * **Pharmacology Link:** **Cyclosporine and Tacrolimus** work by inhibiting calcineurin, which prevents the transcription of IL-2, thereby suppressing T-cell-mediated graft rejection. * **Therapeutic Use:** Recombinant IL-2 (Aldesleukin) is used in the treatment of Metastatic Renal Cell Carcinoma and Melanoma to boost the anti-tumor immune response.

Question 43: Which of the following is a generic term for a protein or glycoprotein released by one cell population that acts as an intercellular mediator?

A. Hormone
B. Cytokine (Correct Answer)
C. Pheromone
D. Antibody

Explanation: ### Explanation **Correct Answer: B. Cytokine** **Why it is correct:** Cytokines are low-molecular-weight, soluble **proteins or glycoproteins** secreted by various cell populations (primarily immune cells like macrophages and T-cells) that act as **intercellular mediators**. They function as signaling molecules that regulate the intensity and duration of the immune response by binding to specific receptors on target cells. They can act in an autocrine (same cell), paracrine (nearby cell), or endocrine (distant cell) fashion. **Analysis of Incorrect Options:** * **A. Hormone:** While hormones are also intercellular mediators, they are typically produced by specialized endocrine glands and travel through the bloodstream to act on distant organs. Unlike cytokines, which are produced by many cell types, hormones have specific glandular origins. * **C. Pheromone:** These are chemical substances produced and released into the **environment** by an animal to affect the behavior or physiology of others of its species. They do not act as internal mediators within a single organism. * **D. Antibody (Immunoglobulin):** These are proteins produced specifically by B-lymphocytes (plasma cells) in response to an antigen. Their primary role is to identify and neutralize foreign objects (like bacteria and viruses) rather than acting as general intercellular signaling mediators. **High-Yield Clinical Pearls for NEET-PG:** * **Pleiotropy:** A single cytokine having different biological effects on different target cells (e.g., IL-4 acting on B-cells, T-cells, and mast cells). * **Redundancy:** Multiple cytokines mediating the same function (e.g., IL-2, IL-4, and IL-5 all stimulating B-cell proliferation). * **Cytokine Storm:** An overproduction of cytokines (like IL-6, TNF-α) leading to systemic inflammation, often seen in severe COVID-19 or Sepsis. * **Key Cytokine:** **IL-1** is the endogenous pyrogen responsible for fever.

Question 44: Cell-mediated immunity is mediated by which of the following?

A. Helper T cells
B. Suppressor T cells
C. Cytotoxic T cells
D. All of the above (Correct Answer)

Explanation: **Explanation:** Cell-mediated immunity (CMI) is an immune response that does not involve antibodies but rather relies on the activation of **T lymphocytes**. It is primarily directed against intracellular pathogens (viruses, fungi, and some bacteria like *M. tuberculosis*), cancer cells, and foreign tissue transplants. The correct answer is **D (All of the above)** because CMI involves a coordinated effort from various T cell subsets: 1. **Helper T cells (CD4+):** These are the "orchestrators." Upon recognizing antigens presented by MHC Class II molecules, they secrete cytokines (like IFN-γ and IL-2) that activate macrophages, B cells, and Cytotoxic T cells. 2. **Cytotoxic T cells (CD8+):** These are the "effectors." They directly kill infected or abnormal cells by releasing perforins and granzymes, recognizing antigens via MHC Class I molecules. 3. **Suppressor/Regulatory T cells (Tregs):** These are essential for "immunological tolerance." They modulate the immune system, maintain self-tolerance, and prevent autoimmune diseases by suppressing excessive CMI responses. **Why individual options are incomplete:** While A, B, and C are all components of CMI, selecting any single one would be incomplete. CMI is a functional system requiring the activation (Helper), execution (Cytotoxic), and regulation (Suppressor) of T-cell-driven responses. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD4+ cells are MHC II restricted; CD8+ cells are MHC I restricted (Rule of 8: 4x2=8 and 8x1=8). * **Delayed-Type Hypersensitivity (Type IV):** This is the classic clinical manifestation of CMI (e.g., Mantoux test, contact dermatitis). * **Cytokine Profile:** Th1 cells (a subset of Helper T cells) are the primary drivers of CMI through the secretion of **IL-2 and IFN-γ**. * **Deficiency:** Patients with impaired CMI (e.g., HIV/AIDS) are highly susceptible to opportunistic infections like *Pneumocystis jirovecii* and *Cryptococcus*.

Question 45: A 34-year-old male patient visits a physician with complaints of fatigue, weight loss, night sweats, and "swollen glands." The physician also observes that he has an oral yeast infection. Which of the following tests would most likely reveal the cause of his problems?

A. A test for CD8 lymphocytes
B. A human T-lymphotropic virus type I (HTLV-I) test
C. An HIV ELISA test (Correct Answer)
D. A test for infectious mononucleosis

Explanation: ### Explanation **Correct Answer: C. An HIV ELISA test** **1. Why it is correct:** The patient presents with the classic triad of **constitutional symptoms** (fatigue, weight loss, night sweats), **generalized lymphadenopathy** ("swollen glands"), and an **opportunistic infection** (oral candidiasis/yeast infection). This clinical picture is highly suggestive of **HIV/AIDS**. In an adult with oral thrush and systemic symptoms, the primary goal is to screen for HIV. The **ELISA (Enzyme-Linked Immunosorbent Assay)** is the standard initial screening test used to detect HIV-1 and HIV-2 antibodies (and p24 antigen in 4th generation assays). **2. Why other options are incorrect:** * **A. CD8 lymphocytes:** While CD8 T-cells are involved in the immune response to viral infections, they are not diagnostic for HIV. In HIV, the hallmark is a depletion of **CD4+ T-cells**, leading to an inverted CD4:CD8 ratio. * **B. HTLV-I test:** HTLV-I is associated with Adult T-cell Leukemia/Lymphoma (ATLL) and Tropical Spastic Paraparesis. While it is a retrovirus, it does not typically present with oral candidiasis and generalized wasting like HIV. * **D. Infectious mononucleosis (EBV):** Mononucleosis presents with fever, sore throat, and lymphadenopathy (usually posterior cervical). However, it is an acute illness and does not typically cause significant weight loss, night sweats, or oral yeast infections (thrush). **3. NEET-PG High-Yield Pearls:** * **Screening vs. Confirmation:** ELISA is the screening test (High Sensitivity). Western Blot was traditionally the confirmatory test (High Specificity), but current protocols often use the **HIV-1/HIV-2 differentiation immunoassay**. * **Window Period:** The time between infection and the appearance of detectable antibodies (usually 3-12 weeks). * **Oral Candidiasis:** In a young, non-diabetic patient not on steroids/antibiotics, oral thrush is an **AIDS-defining clinical condition** until proven otherwise. * **Diagnosis of HIV in Infants (<18 months):** Use **DNA-PCR** (Proviral DNA) because maternal IgG antibodies can cross the placenta, giving a false positive ELISA.

Question 46: MHC class I molecules are represented on which of the following cell types?

A. All cells
B. All nucleated cells (Correct Answer)
C. RBCs
D. None

Explanation: ### Explanation **1. Why "All nucleated cells" is correct:** Major Histocompatibility Complex (MHC) Class I molecules are essential for the immune system to distinguish "self" from "non-self." They are expressed on the surface of **all nucleated cells** and **platelets**. Their primary function is to present endogenous antigens (like viral proteins or tumor antigens) to **CD8+ Cytotoxic T-cells**. Since any nucleated cell in the body is susceptible to viral infection or malignant transformation, they must all possess the machinery to signal the immune system via MHC I. **2. Why the other options are incorrect:** * **Option A (All cells):** This is technically incorrect because it would include Red Blood Cells (RBCs). * **Option C (RBCs):** Mature human RBCs lack a nucleus and the necessary organelles (like the endoplasmic reticulum) to synthesize and express MHC molecules. This is clinically significant as it prevents RBCs from being targeted by cytotoxic T-cells, though it also means they cannot present malarial antigens in the same way. * **Option D (None):** Incorrect, as MHC I expression is a fundamental feature of vertebrate immunity. **3. High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I Structure:** Consists of an **alpha (α) heavy chain** (encoded on Chromosome 6) and a **β2-microglobulin** light chain (encoded on Chromosome 15). * **MHC Class II:** Expressed only on **Professional Antigen-Presenting Cells (APCs)**—namely Dendritic cells, Macrophages, and B-cells. They present exogenous antigens to **CD4+ Helper T-cells**. * **Rule of 8:** * MHC **I** × CD**8** = 8 * MHC **II** × CD**4** = 8 * **Exception:** While platelets are anucleated, they are a notable exception and **do** express MHC Class I.

Question 47: Memory cells do not undergo apoptosis due to the presence of which growth factor?

A. Platelet derived growth factor
B. Nerve growth factor (Correct Answer)
C. Insulin like growth factor
D. Fibroblast growth factor

Explanation: ### Explanation **Correct Option: B. Nerve growth factor (NGF)** The survival of memory B cells is a critical component of long-term immunity. Unlike effector cells, which undergo apoptosis after an immune response, memory cells persist for years. This survival is mediated by the expression of **Nerve Growth Factor (NGF)** and its high-affinity receptor, **TrkA**. NGF acts as an autocrine/paracrine survival factor for memory B cells. It prevents apoptosis by upregulating anti-apoptotic proteins like **Bcl-2** and downregulating pro-apoptotic signals. While NGF is traditionally associated with neuronal growth, its role in the immune system is a high-yield concept for competitive exams, highlighting the cross-talk between the nervous and immune systems. **Analysis of Incorrect Options:** * **A. Platelet-derived growth factor (PDGF):** Primarily involved in wound healing, angiogenesis, and the proliferation of connective tissue/smooth muscle cells. It does not play a role in lymphocyte memory. * **C. Insulin-like growth factor (IGF):** Primarily mediates the effects of growth hormone and promotes systemic cell growth and development, but is not the specific factor responsible for preventing memory cell apoptosis. * **D. Fibroblast growth factor (FGF):** Involved in embryonic development, tissue repair, and tumor growth; it does not regulate the lifespan of memory B cells. **High-Yield Clinical Pearls for NEET-PG:** * **Memory B cells** express **CD27**, which is a classic marker used to distinguish them from naive B cells. * The transition from an activated B cell to a memory cell involves **isotype switching** and **somatic hypermutation** in the germinal centers of secondary lymphoid organs. * **Bcl-2** is the primary intracellular protein that inhibits apoptosis in these cells; its overexpression is also linked to Follicular Lymphoma (t:14,18).

Question 48: Complement attaches to immunoglobulin at which part?

A. Aminoterminal
B. Fab region
C. Variable region
D. Fc fragment (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right (Fc Fragment):** The complement system (specifically the classical pathway) is initiated when the **C1q** component binds to the **CH2 domain** of IgG or the **CH3 domain** of IgM. These domains are located within the **Fc (Fragment crystallizable)** portion of the antibody. The Fc region is responsible for the biological effector functions of immunoglobulins, such as opsonization, placental transfer, and complement fixation, rather than antigen binding. **2. Why the Other Options are Wrong:** * **A. Aminoterminal:** This is the end of the polypeptide chain where the variable regions are located. It is involved in antigen recognition, not complement binding. * **B. Fab region (Fragment antigen-binding):** This region consists of one constant and one variable domain of each of the heavy and light chains. Its primary role is to bind specifically to the antigen. * **C. Variable region:** Located within the Fab region, this area contains the paratope (antigen-binding site). It determines the idiotype of the antibody and does not interact with complement proteins. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Complement Fixation Order:** IgM is the most potent activator of the classical pathway (due to its pentameric structure), followed by IgG3 > IgG1 > IgG2. **IgG4, IgA, IgD, and IgE** do not activate the classical pathway. * **Specific Binding Site:** For IgG, the specific binding site for C1q is the **CH2** domain. For IgM, it is the **CH3** domain. * **Mnemonic:** "C" for **C**omplement binds to the **C**onstant region (**Fc**). * **Alternative Pathway:** Does not require antibodies for activation; it is triggered directly by microbial surfaces (e.g., Endotoxin/LPS).

Question 49: All of the following help in opsonisation except?

A. IgG
B. Lectin
C. C-reactive protein
D. None of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **None of the above** because all three options listed (IgG, Lectin, and C-reactive protein) are established **opsonins**. Opsonization is the process by which "opsonins" coat a pathogen to enhance its recognition and ingestion by phagocytes (neutrophils and macrophages). 1. **IgG (Option A):** This is the most potent serum opsonin. The **Fc portion** of the IgG molecule (specifically IgG1 and IgG3) binds to Fcγ receptors on phagocytes, while the Fab portion binds to the antigen. 2. **Lectin (Option B):** Specifically, **Mannose-Binding Lectin (MBL)** acts as an opsonin. It binds to carbohydrate patterns on microbial surfaces and can directly enhance phagocytosis or activate the Lectin pathway of the complement system. 3. **C-reactive Protein (Option C):** CRP is an acute-phase reactant that acts as a pattern recognition receptor. It binds to phosphocholine on bacterial surfaces and acts as an opsonin, while also activating the classical complement pathway via C1q. **Why "None of the above" is correct:** Since IgG, Lectin, and CRP all facilitate opsonization, there is no "except" among the choices. **High-Yield Clinical Pearls for NEET-PG:** * **Most powerful opsonins:** IgG and **C3b** (the "heat-labile" opsonin). * **Other Opsonins:** C4b, iC3b, Fibronectin, and Surfactant proteins A and D. * **Mechanism:** Opsonins overcome the negative electrostatic charge (zeta potential) between the phagocyte and the bacterium, allowing them to adhere. * **Clinical Correlation:** Patients with splenectomy or complement deficiencies (C3) are at high risk for infections by **encapsulated organisms** (e.g., *S. pneumoniae*) because these bacteria require opsonization to be cleared.

Question 50: Which components of innate immunity are active against viral cells?

A. NK cells (Correct Answer)
B. Cytotoxic cells
C. B-cell
D. Memory B cell

Explanation: **Explanation:** The correct answer is **NK (Natural Killer) cells**. **1. Why NK cells are correct:** NK cells are a critical component of the **innate immune system**. Unlike T or B cells, they do not require prior sensitization. They are specifically designed to target and kill virally infected cells and tumor cells. They function by recognizing the "missing self"—a phenomenon where viruses downregulate **MHC Class I molecules** on the host cell surface to evade T-cells. NK cells detect this absence and induce apoptosis in the target cell via the release of perforins and granzymes. **2. Why other options are incorrect:** * **Cytotoxic T-cells (CD8+):** While these are highly effective against viruses, they are part of **adaptive (acquired) immunity**, not innate immunity. They require antigen presentation via MHC Class I and prior activation. * **B-cells:** These are mediators of **humoral adaptive immunity**. Their primary role is to differentiate into plasma cells to produce antibodies. * **Memory B-cells:** These are specialized B-cells that persist after an infection to provide a rapid response upon re-exposure. They are a hallmark of **adaptive immunity** and immunological memory. **High-Yield Clinical Pearls for NEET-PG:** * **Interferons (IFN-α and IFN-β):** These are the primary cytokines of innate immunity that inhibit viral replication in neighboring cells. * **NK Cell Markers:** CD16 (FcγRIII) and CD56 are the characteristic surface markers used to identify NK cells. * **Mechanism:** NK cells are inhibited by the presence of MHC Class I on healthy cells (via KIR - Killer Immunoglobulin-like Receptors). * **TLRs:** Toll-like receptors (especially TLR 3, 7, 8, and 9) are innate sensors that recognize viral nucleic acids.

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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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Immunology — MCQs

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