Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 161: Which cell type lacks HLA antigens?

A. Monocyte
B. Thrombocytes
C. Neutrophil
D. Red blood cell (Correct Answer)

Explanation: **Explanation:** The Human Leukocyte Antigen (HLA) system is the human version of the **Major Histocompatibility Complex (MHC)**. HLA Class I antigens (HLA-A, B, and C) are expressed on the surface of almost all **nucleated cells** in the body. **1. Why Red Blood Cells (RBCs) are the correct answer:** Mature Red Blood Cells are **non-nucleated** cells. Because they lack a nucleus and the necessary protein-synthesizing machinery, they do not express HLA Class I or Class II antigens on their surface. Instead, RBCs express blood group antigens (ABO and Rh systems). This is why HLA matching is not required for simple blood transfusions, whereas it is critical for organ and bone marrow transplants. **2. Why the other options are incorrect:** * **Monocytes (A) & Neutrophils (C):** These are nucleated white blood cells. As nucleated cells, they express high levels of HLA Class I antigens. Monocytes, being professional antigen-presenting cells (APCs), also express HLA Class II antigens. * **Thrombocytes/Platelets (B):** Although platelets are anucleated fragments of megakaryocytes, they are a notable **exception** to the "nucleated cell" rule. Platelets **do express HLA Class I antigens** on their surface (inherited from the megakaryocyte). This is clinically significant as patients can develop "HLA alloimmunization" after multiple platelet transfusions. **High-Yield NEET-PG Pearls:** * **HLA Class I:** Found on all nucleated cells + Platelets. (Mnemonic: 1 x 8 = 8; interacts with CD8+ T cells). * **HLA Class II:** Found only on professional Antigen Presenting Cells (B-cells, Macrophages, Dendritic cells, and Thymic epithelial cells). (Mnemonic: 2 x 4 = 8; interacts with CD4+ T cells). * **Trophoblasts:** These are another important cell type that lacks classical HLA-A and HLA-B to avoid maternal immune rejection.

Question 162: The binding of complement to a bacterial cell surface is termed as:

A. Opsonization (Correct Answer)
B. Complement activation
C. Complement stabilization
D. None of the above

Explanation: **Explanation:** The correct answer is **Opsonization**. **1. Why Opsonization is correct:** Opsonization is the process by which a pathogen is marked for ingestion and destruction by a phagocyte. In the complement system, **C3b** (and to a lesser extent C4b) acts as a potent **opsonin**. When these complement proteins bind to the bacterial cell surface, they act as "tags." Phagocytic cells, such as macrophages and neutrophils, possess specific receptors (CR1) for C3b. This binding significantly enhances the efficiency of phagocytosis, acting like a "handle" that allows the immune cell to grip and engulf the bacteria. **2. Why other options are incorrect:** * **Complement activation:** This refers to the entire biochemical cascade (Classical, Alternative, or Lectin pathways) that leads to the generation of effector molecules. While binding is a *step* in activation, the specific term for "coating" a cell to enhance phagocytosis is opsonization. * **Complement stabilization:** This is not a standard immunological term for surface binding. In immunology, "stabilization" usually refers to the role of **Properdin**, which stabilizes the C3 convertase (C3bBb) in the alternative pathway, rather than the binding of complement to the bacteria itself. **Clinical Pearls for NEET-PG:** * **Most potent opsonins:** IgG and C3b are the two most important opsonins in the body. * **C3b function:** Remember the mnemonic "C3**b** **B**inds **B**acteria" (Opsonization). * **C5a function:** Primarily involved in **chemotaxis** and inflammation. * **Membrane Attack Complex (MAC):** Formed by C5b-C9; its primary role is the osmotic lysis of Gram-negative bacteria (especially *Neisseria*). * **Deficiency:** Patients with C3 deficiency suffer from recurrent pyogenic infections due to impaired opsonization.

Question 163: Prozone phenomenon is a feature of which of the following diseases?

A. Tularemia
B. Legionnaire's disease
C. Plague
D. Brucellosis (Correct Answer)

Explanation: ### Explanation The **Prozone phenomenon** is a classic immunological concept frequently tested in NEET-PG. It refers to a **false-negative agglutination test** result occurring due to an **excess of antibodies** (hyperantiserum). When antibody concentration is too high, they coat all antigen binding sites individually, preventing the formation of the cross-linked "lattice" required for visible agglutination. **Why Brucellosis is the Correct Answer:** Brucellosis (caused by *Brucella* species) is the quintessential example of a disease exhibiting the prozone phenomenon, particularly in the **Standard Agglutination Test (SAT)**. In chronic cases or intense infections, high titers of **IgA and IgG (blocking antibodies)** interfere with the agglutination of IgM. To overcome this and achieve a correct diagnosis, the serum must be serially diluted to reduce antibody concentration until the "zone of equivalence" is reached, allowing lattice formation. **Analysis of Incorrect Options:** * **Tularemia (*Francisella tularensis*):** While diagnosed via serology (agglutination), it is not classically associated with the prozone phenomenon in standard medical literature. * **Legionnaire's Disease (*Legionella pneumophila*):** Diagnosis is primarily via urinary antigen tests, PCR, or culture (BCYE agar); agglutination-based prozone issues are not a hallmark. * **Plague (*Yersinia pestis*):** Diagnosis relies on microscopy (safety-pin appearance), culture, or F1 antigen detection, rather than tests prone to the prozone effect. **High-Yield Clinical Pearls for NEET-PG:** * **Management of Prozone:** If Brucellosis is clinically suspected but SAT is negative, perform **serial dilutions** of the serum or use the **Coombs Antiglobulin Test** to detect blocking antibodies. * **Post-zone Phenomenon:** This is the opposite—a false negative due to **antigen excess**. * **Brucella Culture:** Uses **Castaneda’s medium** (biphasic medium). * **Rose Bengal Plate Test:** A rapid screening test for Brucellosis.

Question 164: ASLO titres are used in the diagnosis of which condition?

A. Acute rheumatoid arthritis
B. Acute rheumatic fever (Correct Answer)
C. Ankylosing spondylitis
D. Osteoarthritis

Explanation: ### Explanation **Correct Answer: B. Acute Rheumatic Fever** **Underlying Medical Concept:** Antistreptolysin O (ASLO) is an antibody produced against **Streptolysin O**, an oxygen-labile exotoxin secreted by **Group A Beta-hemolytic Streptococci (GABS)**, specifically *Streptococcus pyogenes*. ASLO titers are a marker of a recent streptococcal infection. Acute Rheumatic Fever (ARF) is a non-suppurative, immunologically mediated complication that occurs 2–3 weeks after a streptococcal pharyngitis. According to the **Revised Jones Criteria**, evidence of a preceding streptococcal infection (such as elevated or rising ASLO titers) is an essential requirement for diagnosing ARF (except in cases of chorea or carditis presenting months later). **Why Incorrect Options are Wrong:** * **A. Acute Rheumatoid Arthritis:** This is an autoimmune inflammatory disorder characterized by symmetric small joint involvement. It is diagnosed using Rheumatoid Factor (RF) and Anti-CCP antibodies, not streptococcal markers. * **C. Ankylosing Spondylitis:** This is a seronegative spondyloarthropathy strongly associated with the **HLA-B27** gene. It involves the sacroiliac joints and spine. * **D. Osteoarthritis:** This is a degenerative "wear-and-tear" joint disease related to aging and mechanical stress; it has no infectious or immunological etiology involving ASLO. **High-Yield Clinical Pearls for NEET-PG:** * **Threshold:** A titer of **>200 units** is generally considered significant in adults (333 units in children). * **Timing:** ASLO levels begin to rise 1 week after infection and peak at **3–5 weeks**. * **Limitation:** ASLO titers do **not** rise significantly in streptococcal skin infections (Impetigo/Pyoderma) because skin cholesterol neutralizes Streptolysin O. In such cases, the **Anti-DNase B** test is the investigation of choice. * **Other Markers:** Anti-hyaluronidase and Anti-streptokinase are other tests used in the "Streptozyme" panel.

Question 165: The class of antibodies that plays an important role in type I hypersensitivity reactions is _____,

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

Explanation: **Explanation:** **Correct Answer: C. IgE** Type I hypersensitivity (Immediate Hypersensitivity) is mediated by **IgE antibodies**. Upon initial exposure to an allergen, IgE is produced and binds to high-affinity receptors (**FcεRI**) on the surface of **mast cells and basophils**. On subsequent exposure, the allergen cross-links these membrane-bound IgE molecules, triggering degranulation and the release of pharmacological mediators like **histamine**, leukotrienes, and prostaglandins. This leads to clinical manifestations such as anaphylaxis, asthma, and urticaria. **Why other options are incorrect:** * **IgA:** Primarily found in secretions (tears, saliva, colostrum) and provides mucosal immunity. It does not mediate Type I hypersensitivity. * **IgD:** Acts mainly as a surface receptor on B-cells for antigen recognition; its systemic effector function is minimal. * **IgG:** The most abundant serum antibody, involved in Type II (cytotoxic) and Type III (immune-complex) hypersensitivity. It provides long-term immunity and crosses the placenta. **High-Yield NEET-PG Pearls:** * **Mnemonic for Hypersensitivity:** **ACID** (Type **A**naphyalctic/IgE, Type **C**ytotoxic/IgG, Type **I**mmune-Complex, Type **D**elayed/T-cells). * **Prausnitz-Küstner (PK) Reaction:** A classic test used to demonstrate the presence of IgE (reaginic antibodies) in serum. * **Eosinophilia:** Type I reactions are often associated with an increase in eosinophil count, stimulated by IL-5. * **Casoni’s Test:** A skin test for Hydatid disease that relies on a Type I hypersensitivity mechanism.

Question 166: Which of the following is NOT an example of delayed type hypersensitivity?

A. Arthus phenomenon (Correct Answer)
B. Contact dermatitis
C. Tuberculin test
D. Graft versus host reaction

Explanation: ### Explanation **1. Why Arthus Phenomenon is the Correct Answer:** The **Arthus phenomenon** is a localized **Type III Hypersensitivity** reaction (Immune-complex mediated). It occurs when an antigen is injected into the skin of an individual with high levels of pre-existing circulating IgG antibodies. This leads to the formation of antigen-antibody complexes that deposit in small blood vessel walls, activating the complement system and causing inflammatory vasculitis and tissue necrosis. Unlike delayed-type reactions, it is mediated by antibodies, not T-cells. **2. Analysis of Incorrect Options (Type IV Hypersensitivity):** * **Contact Dermatitis (Option B):** A classic example of Type IV hypersensitivity. It is mediated by CD4+ and CD8+ T-cells reacting to haptens (like nickel or poison ivy) upon re-exposure. * **Tuberculin Test (Option C):** The prototype of Delayed-Type Hypersensitivity (DTH). It involves the recruitment of macrophages by Th1 cells in response to PPD (Purified Protein Derivative), peaking at 48–72 hours. * **Graft versus Host Reaction (Option D):** This involves donor T-cells recognizing and attacking the recipient’s (host) tissues. It is a cell-mediated immune response, falling under the spectrum of Type IV reactions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Coombs and Gell Classification:** * **Type I:** Immediate (IgE) * **Type II:** Cytotoxic (IgG/IgM) * **Type III:** Immune Complex (Arthus, Serum Sickness) * **Type IV:** Delayed/Cell-mediated (T-cells) * **Memory Aid:** **"ACID"** (Anaphylactic, Cytotoxic, Immune-complex, Delayed). * **Arthus vs. Serum Sickness:** Arthus is **localized** (e.g., post-vaccination swelling), while Serum Sickness is **systemic** (e.g., fever, rash, arthralgia after antitoxin administration). Both are Type III.

Question 167: Killer cells are associated with which type of immunologic response?

A. Type I
B. Type II
C. Type III
D. None of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **None of the above** because "Killer cells" (specifically Natural Killer or NK cells) are primary mediators of **Type IV Hypersensitivity** (Cell-mediated immunity), which is not listed among the options. **1. Why "None of the above" is correct:** Killer cells, including **Natural Killer (NK) cells** and **Cytotoxic T-lymphocytes (CD8+ T cells)**, are the hallmark of cell-mediated immune responses. In the Gell and Coombs classification, Type IV hypersensitivity is the only "delayed-type" response that does not involve antibodies; instead, it relies on T-cells and NK cells to induce direct cytotoxicity or cytokine-mediated inflammation. **2. Why other options are incorrect:** * **Type I (Immediate):** Mediated by **IgE antibodies** and mast cell degranulation (e.g., Anaphylaxis, Asthma). * **Type II (Cytotoxic):** Mediated by **IgG or IgM antibodies** directed against antigens on specific cell surfaces (e.g., ABO incompatibility, Myasthenia Gravis). While NK cells can participate here via Antibody-Dependent Cellular Cytotoxicity (ADCC), the primary mechanism is antibody-driven. * **Type III (Immune-complex):** Mediated by the deposition of **antigen-antibody complexes** in tissues, leading to complement activation (e.g., SLE, Serum sickness). **High-Yield Clinical Pearls for NEET-PG:** * **NK Cells:** Large granular lymphocytes that do not require prior sensitization. They recognize cells lacking **MHC Class I** molecules ("Missing Self" hypothesis). * **ADCC:** A bridge between humoral and innate immunity where NK cells kill target cells coated with IgG via the **CD16 receptor** (FcγRIII). * **Type IV Subtypes:** Remember that Type IV is subdivided (IVa to IVd) based on the specific cell type involved (Th1, Th2, Cytotoxic T-cells, or Neutrophils).

Question 168: Which of the following is NOT a component of innate immunity?

A. Epithelial surfaces
B. Antibody (Correct Answer)
C. Lysozyme
D. Sebum

Explanation: **Explanation:** Innate immunity is the body's first line of defense, providing a non-specific, rapid response that is present from birth. It lacks memory and does not improve with repeated exposure. **Why Antibody is the Correct Answer:** Antibodies (Immunoglobulins) are components of **Adaptive (Acquired) Immunity**. They are produced by B-lymphocytes (plasma cells) in response to specific antigens. Unlike innate components, antibodies are highly specific, involve a lag period for initial production, and generate immunological memory. **Why the other options are part of Innate Immunity:** * **Epithelial surfaces (Option A):** These act as **physical/mechanical barriers**. The skin and mucous membranes prevent the entry of pathogens through shedding (desquamation) and ciliary movement. * **Lysozyme (Option C):** This is a **chemical/physiological barrier**. It is an enzyme found in tears, saliva, and nasal secretions that kills bacteria by hydrolyzing the peptidoglycan layer of the cell wall. * **Sebum (Option D):** Produced by sebaceous glands, sebum contains long-chain fatty acids that create an acidic pH (3-5) on the skin, inhibiting the growth of many pathogenic bacteria and fungi. **High-Yield Clinical Pearls for NEET-PG:** * **Components of Innate Immunity:** Physical barriers (Skin/Mucosa), Chemical barriers (pH, Lysozyme, Complement), Cellular barriers (Phagocytes, NK cells), and Cytokines (Interferons). * **NK Cells:** These are the only lymphocytes that are part of the **innate** immune system. * **Complement System:** While it bridges both systems, the **Alternative and Lectin pathways** are considered part of innate immunity, whereas the Classical pathway (antibody-dependent) is part of adaptive immunity. * **TLRs (Toll-Like Receptors):** These are key PRRs (Pattern Recognition Receptors) in innate immunity that recognize PAMPs on pathogens.

Question 169: CD4 cells are involved in all of the following processes, EXCEPT:

A. Acting as a helper function for B cells
B. Processing and presenting antigens (Correct Answer)
C. Producing and releasing interleukin-2
D. Producing and releasing interferon-gamma

Explanation: ### Explanation The correct answer is **B. Processing and presenting antigens.** **1. Why Option B is correct:** CD4+ T cells (Helper T cells) are the **recipients** of antigen presentation, not the presenters. Antigen processing and presentation is the function of **Antigen-Presenting Cells (APCs)** such as Dendritic cells, Macrophages, and B cells. These APCs process exogenous antigens and present them via **MHC Class II** molecules to the T-cell receptor (TCR) on CD4 cells. CD4 cells then become activated to coordinate the immune response. **2. Why the other options are incorrect:** * **Option A:** CD4 cells (specifically Th2 subset) provide "help" to B cells by releasing cytokines (like IL-4, IL-5) and through CD40-CD40L interaction, which is essential for B cell activation, isotype switching, and memory cell formation. * **Option C:** Upon activation, CD4 cells (specifically Th1 subset) produce **Interleukin-2 (IL-2)**, which acts as an autocrine growth factor to stimulate T-cell proliferation (clonal expansion). * **Option D:** Activated Th1 cells produce **Interferon-gamma (IFN-γ)**, which is the primary cytokine responsible for activating macrophages and enhancing their microbicidal activity. **3. High-Yield Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD4 cells recognize antigens only in association with **MHC Class II** (Rule of 8: 4 × 2 = 8), while CD8 cells recognize **MHC Class I** (8 × 1 = 8). * **Th1 vs. Th2:** Th1 cells primarily mediate **Cell-Mediated Immunity** (IFN-γ, IL-2, TNF-β), while Th2 cells mediate **Humoral Immunity** (IL-4, IL-5, IL-10, IL-13). * **HIV Pathogenesis:** HIV selectively infects and depletes CD4+ T cells by binding to the CD4 molecule and CCR5/CXCR4 co-receptors, leading to profound immunodeficiency.

Question 170: Which of the following interleukins is NOT primarily produced by T cells?

A. Interleukin 1 (Correct Answer)
B. Interleukin 2
C. Interleukin 4
D. Interleukin 5

Explanation: **Explanation:** The correct answer is **Interleukin 1 (IL-1)**. The fundamental concept here is distinguishing between cytokines produced by innate immune cells (monocytes/macrophages) and those produced by adaptive immune cells (T-lymphocytes). * **Interleukin 1 (IL-1):** This is a pro-inflammatory cytokine primarily produced by **activated macrophages**, monocytes, and dendritic cells. It acts as an endogenous pyrogen (inducing fever) and stimulates T-cell activation. It is a hallmark of the innate immune response rather than a T-cell product. * **Interleukin 2 (IL-2):** Produced primarily by **Th1 cells**. It is known as the "T-cell growth factor," essential for the proliferation and clonal expansion of T and B lymphocytes. * **Interleukin 4 (IL-4):** Produced by **Th2 cells**. It promotes B-cell differentiation into plasma cells and mediates the "class switching" of antibodies to IgE. * **Interleukin 5 (IL-5):** Also produced by **Th2 cells**. Its primary role is the recruitment and activation of eosinophils, making it crucial in parasitic infections and allergic reactions. **High-Yield NEET-PG Pearls:** * **Hot T-BONE Steak:** A classic mnemonic for IL functions: * **IL-1:** **Hot** (Fever) * **IL-2:** Stimulates **T** cells * **IL-3:** Stimulates **B**one marrow * **IL-4:** Stimulates Ig**E** production * **IL-5:** Stimulates Ig**A** production * **IL-8:** The primary chemotactic factor for **neutrophils** ("Clean up on aisle 8"). * **IL-10 & TGF-β:** The major "anti-inflammatory" cytokines that downregulate the immune response.

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Cells and Organs of Immune System

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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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