Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 531: Cachectin is produced by which type of cell?

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

Explanation: **Explanation:** **Cachectin** is the historical name for **Tumor Necrosis Factor-alpha (TNF-α)**. It was originally named "cachectin" because of its role in causing **cachexia** (profound weight loss and muscle wasting) in patients with chronic infections and malignancies. 1. **Why Macrophages are correct:** TNF-α (Cachectin) is a potent pro-inflammatory cytokine primarily produced by **activated macrophages** and monocytes. It is released in response to stimuli like Lipopolysaccharide (LPS/Endotoxin) from Gram-negative bacteria. It plays a central role in the systemic inflammatory response, recruitment of immune cells, and the induction of fever (endogenous pyrogen). 2. **Why other options are incorrect:** * **Neutrophils:** While neutrophils are key players in acute inflammation and respond to TNF-α, they are not the primary source of its production. * **Eosinophils:** These cells are primarily involved in parasitic infections and allergic reactions (Type I Hypersensitivity). Their primary mediators include Major Basic Protein and Eosinophil Cationic Protein. * **Basophils:** These are circulating granulocytes involved in immediate hypersensitivity reactions, primarily releasing histamine and heparin. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Cachexia:** TNF-α causes wasting by suppressing lipoprotein lipase (LPL), leading to the inhibition of triglyceride storage in adipose tissue. * **Septic Shock:** TNF-α is the **principal mediator** of the inflammatory response in septic shock. * **Granuloma Formation:** TNF-α is essential for the formation and maintenance of granulomas (e.g., in Tuberculosis). This is why anti-TNF drugs (like Infliximab or Etanercept) can lead to the reactivation of latent TB. * **Pyrogen:** Along with IL-1 and IL-6, TNF-α acts on the hypothalamus to induce fever.

Question 532: All of the following about NK cells are true, except:

A. Derived from large granular cells
B. Comprise about 5% of human peripheral lymphoid cells
C. Do not secrete interferon-gamma (IFN-gamma) (Correct Answer)
D. Express IgG Fc receptors

Explanation: **Explanation:** Natural Killer (NK) cells are a critical component of the innate immune system. The correct answer is **C** because it is a false statement: **NK cells are major producers of Interferon-gamma (IFN-γ).** Upon activation by IL-12 (from macrophages), NK cells secrete IFN-γ to activate macrophages, creating a bidirectional feedback loop essential for controlling intracellular pathogens. **Analysis of Options:** * **Option A (Derived from large granular cells):** This is true. Morphologically, NK cells are identified as **Large Granular Lymphocytes (LGLs)**. They contain prominent cytoplasmic granules (perforins and granzymes) used to induce apoptosis in target cells. * **Option B (Comprise about 5% of peripheral lymphoid cells):** This is true. NK cells typically constitute **5–15%** of the circulating lymphocyte population in humans. * **Option D (Express IgG Fc receptors):** This is true. NK cells express **CD16**, which is a low-affinity Fc receptor for IgG (FcγRIII). This allows them to bind to antibody-coated target cells and execute **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. **High-Yield Clinical Pearls for NEET-PG:** * **Surface Markers:** NK cells are characterized as **CD3 negative, CD16 positive, and CD56 positive.** * **MHC Restriction:** Unlike T-cells, NK cells are **not MHC-restricted**. They follow the "Missing Self" hypothesis, where they kill cells that have downregulated MHC-I (a common viral/tumor escape mechanism). * **Receptors:** They possess **KIR (Killer Immunoglobulin-like Receptors)** which provide inhibitory signals when they bind to self-MHC-I molecules. * **Origin:** They share a Common Lymphoid Progenitor (CLP) with B and T cells but do not undergo thymic maturation.

Question 533: Which of the following is a pan T lymphocyte marker?

A. CD2
B. CD3 (Correct Answer)
C. CD19
D. CD25

Explanation: **Explanation:** **CD3** is the definitive **pan-T lymphocyte marker** because it is physically associated with the T-cell receptor (TCR). It is expressed on all mature T cells (both Helper T cells and Cytotoxic T cells) and is essential for signal transduction following antigen recognition. In clinical practice, CD3 is used in immunohistochemistry and flow cytometry to identify cells of T-cell lineage. **Analysis of Incorrect Options:** * **CD2:** While CD2 is found on T cells and Natural Killer (NK) cells, it is primarily known as the **LFA-2** (Lymphocyte Function-associated Antigen-2) and is the receptor for sheep red blood cells (responsible for the **E-rosette formation**). It is not as specific a lineage marker as CD3. * **CD19:** This is a classic **pan-B lymphocyte marker**. It is expressed on B cells from the earliest stages of development until they differentiate into plasma cells. * **CD25:** This is the alpha chain of the **IL-2 receptor**. It is a marker of **T-cell activation** and is constitutively expressed on **Regulatory T cells (Tregs)**, rather than all T cells. **High-Yield Clinical Pearls for NEET-PG:** * **Pan-B cell markers:** CD19, CD20, CD21 (CR2 - receptor for EBV). * **NK cell markers:** CD16 (FcγRIII) and CD56. * **HSC marker:** CD34 (Hematopoietic Stem Cell). * **Monocyte/Macrophage marker:** CD14. * **Memory T-cell marker:** CD45RO ("O" for Old). * **Naive T-cell marker:** CD45RA ("A" for Always new).

Question 534: Which cells are involved in antibody-dependent cellular cytotoxicity (ADCC)?

A. NK cell
B. NK cell only
C. Macrophage
D. NK cells, neutrophils, and macrophages (Correct Answer)

Explanation: **Explanation:** Antibody-dependent cellular cytotoxicity (ADCC) is a mechanism of cell-mediated immune defense whereby an effector cell of the immune system actively lyses a target cell, whose membrane-surface antigens have been bound by specific antibodies (usually IgG). **1. Why Option D is Correct:** The hallmark of ADCC is the presence of **Fc receptors (FcR)** on the effector cells. When IgG antibodies bind to a target (like a virus-infected cell or tumor cell), the effector cells recognize the Fc portion of the antibody via their surface receptors. While **Natural Killer (NK) cells** are the primary mediators of ADCC (via CD16/FcγRIII), other cells possessing Fc receptors also participate, including **macrophages, neutrophils, and eosinophils**. Therefore, Option D is the most comprehensive and accurate choice. **2. Analysis of Incorrect Options:** * **Options A & B:** While NK cells are the most frequent "textbook" example of ADCC, they are not the *only* cells involved. In the context of NEET-PG, if a "most complete" list is provided, it is the preferred answer over a single cell type. **3. NEET-PG High-Yield Pearls:** * **Primary Antibody:** IgG is the most common antibody involved in ADCC. * **Eosinophils:** Specifically mediate ADCC against helminths (parasites) using IgE. * **NK Cell Marker:** CD16 is the specific Fc receptor (FcγRIII) on NK cells responsible for ADCC. * **Mechanism:** Unlike phagocytosis, ADCC does not require the ingestion of the target; instead, effector cells release cytotoxic granules (perforins/granzymes) or lytic enzymes directly onto the target cell surface.

Question 535: Cell-mediated immunity is NOT responsible for which of the following?

A. Arthus reaction (Correct Answer)
B. Contact dermatitis
C. Graft rejection
D. Tumor rejection

Explanation: **Explanation:** The core of this question lies in distinguishing between **Type III** and **Type IV hypersensitivity reactions**. **1. Why Arthus Reaction is the Correct Answer:** The Arthus reaction is a localized **Type III hypersensitivity reaction**. It is mediated by **humoral immunity**, specifically the formation of **antigen-antibody (IgG) complexes** that deposit in vessel walls. This triggers the complement cascade and attracts neutrophils, leading to vasculitis and necrosis. Since it depends on antibodies and not T-cells, it is NOT a manifestation of cell-mediated immunity (CMI). **2. Analysis of Incorrect Options (CMI-mediated):** * **Contact Dermatitis (Option B):** This is a classic **Type IV (Delayed-type) hypersensitivity** reaction. It is mediated by sensitized T-lymphocytes (CD4+ and CD8+) reacting to haptens like nickel or poison ivy. * **Graft Rejection (Option C):** Acute and chronic cellular rejections are primarily mediated by **T-cells** (CD8+ cytotoxic T-cells and CD4+ Th1 cells) recognizing foreign MHC molecules. * **Tumor Rejection (Option D):** The immune system’s primary defense against tumors is **Immune Surveillance**, which relies heavily on CMI, specifically Cytotoxic T-lymphocytes (CTLs), Natural Killer (NK) cells, and activated macrophages. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity:** **ACID** (Type I: **A**naphylactic; Type II: **C**ytotoxic; Type III: **I**mmune-Complex; Type IV: **D**elayed/Cell-mediated). * **Arthus Reaction vs. Serum Sickness:** Both are Type III. Arthus is **localized** (e.g., post-vaccination swelling), while Serum Sickness is **systemic**. * **Type IV Hypersensitivity Examples:** Mantoux test (Tuberculin), Lepromin test, Sarcoidosis (granuloma formation), and Type 1 Diabetes (beta-cell destruction).

Question 536: Secondary allograft rejection is primarily mediated by which component of the immune system?

A. Memory cells (Correct Answer)
B. Antibodies
C. Immune complexes
D. None of the above

Explanation: **Explanation:** The correct answer is **Memory cells**. Allograft rejection is a classic example of cell-mediated immunity (CMI). **Why Memory Cells are correct:** When an individual is exposed to a foreign tissue graft for the first time, the immune system undergoes a "Primary Response" (First-set rejection), leading to the formation of sensitized T-lymphocytes and **Memory T-cells**. Upon subsequent exposure to the same donor antigens (a second graft), these pre-existing memory cells recognize the antigens immediately. This triggers a "Secondary Response" known as **Second-set rejection**, which is much faster and more vigorous than the first. This accelerated reaction is the hallmark of immunological memory. **Why other options are incorrect:** * **Antibodies:** While antibodies play a role in Hyperacute rejection (pre-formed antibodies) and some forms of chronic rejection, the classic "Second-set" accelerated rejection is primarily a T-cell mediated process. * **Immune complexes:** These are involved in Type III hypersensitivity reactions (like Serum Sickness or Arthus reaction) but are not the primary mediators of the cellular destruction seen in secondary allograft rejection. **High-Yield Clinical Pearls for NEET-PG:** * **First-set Rejection:** Occurs in 10–14 days (Primary immune response). * **Second-set Rejection:** Occurs in 5–6 days (Secondary immune response mediated by memory T-cells). * **Hyperacute Rejection:** Occurs within minutes to hours; mediated by **pre-formed humoral antibodies** against ABO or HLA antigens. * **Graft vs Host Disease (GVHD):** Occurs when immunocompetent T-cells in the *graft* attack the *host* (common in bone marrow transplants).

Question 537: Vaccination is based on which principle?

A. Agglutination
B. Phagocytosis
C. Immunologic Memory (Correct Answer)
D. Clonal Detection

Explanation: ### Explanation **Correct Answer: C. Immunologic Memory** **Why it is correct:** Vaccination (Active Immunization) is fundamentally based on the principle of **immunologic memory**. When a vaccine (containing weakened, killed, or subunit antigens) is administered, it triggers a **primary immune response**. This leads to the production of antibodies and, more importantly, the generation of long-lived **Memory B and T cells**. Upon subsequent exposure to the actual pathogen, these memory cells recognize the antigen immediately, mounting a **secondary immune response** that is faster, more intense, and more effective, thereby preventing clinical disease. **Why other options are incorrect:** * **Agglutination:** This is an *in vitro* laboratory phenomenon where antibodies cross-link with particulate antigens (like bacteria or RBCs) to form visible clumps. It is a diagnostic tool, not the underlying principle of vaccine efficacy. * **Phagocytosis:** This is a non-specific process of the innate immune system where cells like macrophages and neutrophils engulf pathogens. While it helps in antigen presentation, it does not provide long-term immunity. * **Clonal Detection:** This is a distractor term. The relevant concept is **Clonal Selection**, which describes how specific lymphocytes are activated and proliferated during an immune response, but the ultimate goal of vaccination is the "memory" resulting from that selection. **High-Yield Clinical Pearls for NEET-PG:** * **Primary vs. Secondary Response:** The primary response is dominated by **IgM**, while the secondary response is faster and dominated by **IgG** due to memory cells. * **Live Attenuated Vaccines:** These generally provide better and longer-lasting immunologic memory (often lifelong) compared to killed vaccines because they mimic a natural infection. * **Adjuvants:** Substances (like Alum) added to vaccines to enhance the immune response by stimulating the innate system to better facilitate the development of memory.

Question 538: Interleukin-5 (IL-5) is released in which type of hypersensitivity reaction?

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

Explanation: **Explanation:** **Why Type I is Correct:** Type I Hypersensitivity (Immediate/Anaphylactic) is mediated by **IgE antibodies** and **Th2 cells**. Upon exposure to an allergen, Th2 cells secrete a specific profile of cytokines: * **IL-4:** Stimulates B-cell class switching to IgE. * **IL-5:** Crucial for the **recruitment, activation, and survival of eosinophils**, which are hallmark effector cells in late-phase Type I reactions (e.g., bronchial asthma). * **IL-13:** Stimulates mucus secretion. Since IL-5 is the primary driver for eosinophilia in allergic responses, it is fundamentally linked to Type I reactions. **Why Other Options are Incorrect:** * **Type II (Antibody-mediated):** Involves IgG or IgM binding to cell surface antigens, leading to complement activation or ADCC (e.g., Autoimmune Hemolytic Anemia). It does not primarily involve Th2-derived IL-5. * **Type III (Immune-complex):** Caused by the deposition of antigen-antibody complexes in tissues (e.g., SLE, Arthus reaction). The primary mediators are complement (C5a) and neutrophils. * **Type IV (Delayed-type):** Cell-mediated immunity involving Th1 cells (secreting IFN-γ) or CD8+ T cells. While some subtypes (Type IVb) involve IL-5 and eosinophils (e.g., DRESS syndrome), for NEET-PG purposes, IL-5 is classically associated with the Th2 response of Type I Hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Mepolizumab/Reslizumab:** Monoclonal antibodies against **IL-5** used in severe eosinophilic asthma. * **Benralizumab:** Acts against the **IL-5 receptor**. * **Key Cytokine "Rule of Thumb":** Th1 = IFN-γ, IL-2 (Type IV); Th2 = IL-4, IL-5, IL-13 (Type I). * **Eosinophils** are the characteristic cells of the **late-phase** response in Type I hypersensitivity.

Question 539: Which of the following statements is false regarding innate immunity?

A. Immune response occurs in minutes.
B. Immunological memory responses are absent.
C. Depends on species, race, and individual.
D. Prior exposure to an antigen is required. (Correct Answer)

Explanation: ### Explanation **Innate immunity** is the first line of defense that is present from birth. It provides a non-specific, rapid response to pathogens without requiring prior sensitization. **Why Option D is the Correct Answer (False Statement):** Unlike adaptive (acquired) immunity, innate immunity **does not require prior exposure** to an antigen. It relies on germline-encoded receptors (like Pattern Recognition Receptors or PRRs) to recognize broad, conserved molecular patterns (PAMPs) on microbes. Because it is pre-formed, it is ready to act immediately upon the first encounter with a pathogen. **Analysis of Incorrect Options (True Statements):** * **Option A:** The response occurs in **minutes to hours**. Since the components (neutrophils, macrophages, complement proteins) are already circulating, there is no "lag period" for clonal expansion. * **Option B:** It lacks **immunological memory**. Every encounter with the same pathogen triggers the same magnitude of response; it does not "improve" or become faster upon re-exposure. * **Option C:** It is influenced by **host factors**. Innate resistance varies across **Species** (e.g., humans are immune to distemper), **Race** (e.g., people with sickle cell trait have innate resistance to *P. falciparum*), and **Individuals** (genetic variations in TLRs or complement). **High-Yield Clinical Pearls for NEET-PG:** * **Key Components:** Physical barriers (skin/mucosa), Cells (NK cells, Neutrophils, Macrophages, Dendritic cells), and Humoral factors (Complement, Interferons, CRP). * **NK Cells:** These are the only lymphocytes that are part of the **innate** immune system. * **PRRs:** Toll-like Receptors (TLRs) are classic examples of innate receptors; **TLR-4** recognizes Endotoxin (LPS) of Gram-negative bacteria. * **Diversity:** Innate immunity has **limited diversity** compared to the highly specific V(D)J recombination seen in adaptive immunity.

Question 540: All of the following are true about endotoxins except:

A. Lipopolysaccharides in nature
B. Circulate in blood
C. Highly antigenic (Correct Answer)
D. Induce IL1 and TNF

Explanation: **Explanation:** The correct answer is **C (Highly antigenic)** because endotoxins are actually **poorly antigenic**. Unlike exotoxins, which are proteins that induce high-titer antibody production (antitoxins), endotoxins are lipopolysaccharides (LPS). Their structure does not trigger a strong adaptive immune response, making it impossible to convert them into toxoids for vaccines. **Analysis of Options:** * **A. Lipopolysaccharides in nature:** This is true. Endotoxins are integral components of the outer membrane of Gram-negative bacteria. The **Lipid A** component is responsible for the toxicity. * **B. Circulate in blood:** This is true. During Gram-negative septicemia, endotoxins are released into the bloodstream (endotoxemia) upon bacterial cell lysis or during cell division. * **D. Induce IL-1 and TNF:** This is true. Endotoxins are potent activators of macrophages and monocytes via the **TLR-4 receptor**. This triggers the release of pyrogenic cytokines like **IL-1 and TNF-α**, leading to fever, hypotension, and DIC (Disseminated Intravascular Coagulation). **High-Yield Clinical Pearls for NEET-PG:** * **Heat Stability:** Endotoxins are heat-stable (withstand 100°C for 1 hour), whereas most exotoxins are heat-labile. * **LAL Test:** The **Limulus Amebocyte Lysate (LAL) test** is the specific test used to detect and quantify endotoxins in parenteral solutions. * **Schwartzman Reaction:** This is a classic phenomenon associated with endotoxin release, characterized by localized or systemic tissue necrosis. * **Key Difference:** Exotoxins have specific pharmacological actions (e.g., tetanus causes spastic paralysis), while endotoxins produce non-specific systemic effects (fever, shock).

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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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Transplantation Immunology

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Tumor Immunology

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Immunology — MCQs

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