Immunology — MCQs

Immunology Indian Medical PG Practice Questions and MCQs

Question 581: Type II hypersensitivity is mediated by which component?

A. Complement-mediated
B. Antibody-mediated (Correct Answer)
C. Immune complex-mediated
D. Cell-mediated

Explanation: **Explanation:** Type II hypersensitivity is primarily defined as **Antibody-mediated (Cytotoxic) hypersensitivity**. It occurs when IgG or IgM antibodies bind to specific antigens located on the surface of cells or within the extracellular matrix. This binding leads to cell destruction or dysfunction through three main pathways: opsonization/phagocytosis, complement-mediated lysis, or antibody-dependent cellular cytotoxicity (ADCC). **Analysis of Options:** * **Option B (Correct):** The hallmark of Type II is the direct binding of antibodies to fixed antigens on target cells. Examples include Autoimmune Hemolytic Anemia and Myasthenia Gravis. * **Option A (Incorrect):** While the **Complement system** is often *activated* during a Type II reaction (leading to the Membrane Attack Complex), it is an effector mechanism triggered by the initial antibody binding, not the primary mediator itself. * **Option C (Incorrect):** **Immune complex-mediated** refers to **Type III hypersensitivity**, where soluble antigen-antibody complexes circulate and deposit in tissues (e.g., SLE, Serum Sickness). * **Option D (Incorrect):** **Cell-mediated** refers to **Type IV (Delayed) hypersensitivity**, which involves T-lymphocytes and macrophages rather than antibodies (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic (ACID):** **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed (IV). * **Key Examples of Type II:** Erythroblastosis Fetalis (Rh incompatibility), Goodpasture syndrome, Pemphigus vulgaris, and Rheumatic fever. * **Distinction:** Type II involves **fixed** antigens; Type III involves **soluble** antigens. * **Special Type II:** Graves’ disease and Myasthenia Gravis are "Type II non-cytotoxic" because the antibody alters cell function without killing the cell.

Question 582: A patient presents with a wound on his leg. It heals six weeks later. Which of the following mediators is involved in promoting wound healing?

A. TGF-Beta (Correct Answer)
B. TNF-Alpha
C. INF-Beta
D. IFN-Alpha

Explanation: **Explanation:** **TGF-Beta (Transforming Growth Factor-Beta)** is the correct answer because it is the most critical cytokine involved in the **proliferative and remodeling phases** of wound healing. It acts as a potent fibrogenic agent by: 1. Stimulating the chemotaxis and proliferation of fibroblasts. 2. Increasing the synthesis of collagen and fibronectin while decreasing the degradation of the extracellular matrix (ECM) by inhibiting metalloproteinases. 3. Promoting angiogenesis and epithelialization. **Analysis of Incorrect Options:** * **TNF-Alpha (Tumor Necrosis Factor-Alpha):** This is a potent pro-inflammatory cytokine produced by macrophages. While it is involved in the initial inflammatory phase of wound healing, its chronic elevation actually impairs healing and is associated with chronic non-healing ulcers. * **IFN-Alpha & IFN-Beta (Type I Interferons):** These are primarily involved in innate antiviral immunity and the activation of MHC class I expression. They do not play a direct role in promoting collagen synthesis or tissue repair; in fact, interferons can sometimes inhibit fibroblast proliferation. **NEET-PG High-Yield Pearls:** * **TGF-Beta** is also known for its role in **limiting inflammation** (anti-inflammatory) and is a key mediator in the development of fibrosis in chronic organs (e.g., liver cirrhosis, pulmonary fibrosis). * **Platelet-Derived Growth Factor (PDGF)** is another high-yield mediator that works alongside TGF-Beta to trigger fibroblast migration and smooth muscle proliferation. * **Vitamin C and Zinc** are essential cofactors for collagen synthesis during the remodeling phase; deficiency leads to poor wound healing.

Question 583: Which of the following conditions represents a disorder of T-cell function?

A. Bruton disease
B. Purine nucleoside phosphorylase (PNP) deficiency (Correct Answer)
C. Chediak-Higashi Syndrome
D. Job's Syndrome

Explanation: ### Explanation **Correct Answer: B. Purine nucleoside phosphorylase (PNP) deficiency** **Mechanism:** Purine nucleoside phosphorylase (PNP) is an enzyme involved in the purine salvage pathway. Its deficiency leads to the accumulation of toxic metabolites (specifically deoxyguanosine triphosphate, dGTP) within lymphocytes. **T-cells are uniquely sensitive** to these metabolites, leading to their progressive depletion and dysfunction. While B-cell function remains relatively preserved or only mildly affected, the primary defect is a **profound cell-mediated (T-cell) immunodeficiency**. **Analysis of Incorrect Options:** * **A. Bruton disease (X-linked Agammaglobulinemia):** This is a pure **B-cell defect** caused by a mutation in the Bruton Tyrosine Kinase (BTK) gene, leading to a failure of B-cell maturation and absent antibodies. T-cell function is normal. * **C. Chediak-Higashi Syndrome:** This is a **phagocyte effector defect** (autosomal recessive). It involves a defect in lysosomal trafficking (LYST gene), leading to giant granules in neutrophils and impaired chemotaxis/degranulation, not a primary T-cell disorder. * **D. Job’s Syndrome (Hyper-IgE Syndrome):** This is primarily a defect in **neutrophil chemotaxis** due to STAT3 mutations. While it involves Th17 cell deficiency, it is classically categorized under "defects in phagocyte function" or "combined immunodeficiency" with distinct clinical features like cold abscesses and coarse facies. **NEET-PG High-Yield Pearls:** * **PNP vs. ADA Deficiency:** Adenosine Deaminase (ADA) deficiency causes **SCID** (both B and T cell loss), whereas PNP deficiency primarily affects **T-cells**. * **PNP Clinical Presentation:** Recurrent viral/fungal infections, failure to thrive, and frequently associated **neurologic symptoms** (spasticity, developmental delay). * **Diagnostic Marker:** Low serum uric acid levels are often seen in PNP deficiency due to the block in the purine pathway.

Question 584: At what age does the capacity for producing IgG develop?

A. 6 months (Correct Answer)
B. 1 year
C. 2 years
D. 3 years

Explanation: **Explanation:** The development of the humoral immune system in a neonate follows a specific chronological pattern. At birth, the infant has high levels of **maternal IgG**, which is actively transported across the placenta during the third trimester. This passive immunity provides protection for the first few months of life. **Why 6 months is correct:** Endogenous production of IgG (the infant's own antibodies) begins shortly after birth, but it remains at low levels while maternal IgG is still dominant. Maternal IgG levels begin to decline significantly around 3–4 months. By **6 months of age**, the infant’s own lymphoid system matures sufficiently to take over, and the capacity for significant endogenous IgG production is firmly established. This transition period (3–6 months) is known as the period of **"Physiological Hypogammaglobulinemia."** **Why other options are incorrect:** * **1 year:** By this age, the infant’s IgG levels are already approximately 60% of adult levels. The *capacity* to produce it starts much earlier. * **2 and 3 years:** These ages represent milestones for other isotopes. For example, adult levels of IgG are reached by 5–8 years, while IgA (the slowest to develop) takes until puberty to reach adult levels. **High-Yield Clinical Pearls for NEET-PG:** * **IgM:** The first immunoglobulin produced by the fetus (starts at 20 weeks gestation). Elevated IgM at birth indicates **intrauterine infection** (TORCH), as IgM does not cross the placenta. * **IgA:** Present in colostrum/breast milk, providing local mucosal immunity, but endogenous production is the slowest to reach adult levels. * **Placental Transfer:** Only **IgG** crosses the placenta (specifically via neonatal Fc receptors, FcRn). * **Transient Hypogammaglobulinemia of Infancy:** A condition where the infant’s endogenous IgG production is delayed beyond the normal 6-month mark, leading to recurrent infections.

Question 585: Which of the following statements regarding agglutination reaction is NOT true?

A. It is less sensitive than precipitation reaction for detecting antibodies. (Correct Answer)
B. It works on the same principle as that of precipitation reaction.
C. It is the method used for cross-matching and blood grouping.
D. Agglutination occurs optimally when antigens and antibody react in equivalent proportions.

Explanation: ### Explanation **1. Why Option A is the correct answer (The False Statement):** In immunology, **agglutination is significantly more sensitive than precipitation** for detecting antibodies. This is because the antigen in agglutination is **particulate** (e.g., bacteria, RBCs, or latex beads). When antibodies bind to these large particles, they form visible clumps even at very low concentrations. In contrast, precipitation involves **soluble** antigens, which require a much higher concentration of both antigen and antibody to form a visible lattice. Therefore, the statement that agglutination is "less sensitive" is incorrect. **2. Analysis of Incorrect Options (True Statements):** * **Option B:** Both reactions follow the **Lattice Hypothesis** (Marrack’s Law), where multivalent antigens and antibodies cross-link to form a complex structure. * **Option C:** This is a classic clinical application. Blood grouping (ABO/Rh) and cross-matching utilize **Hemagglutination** to identify surface antigens on RBCs. * **Option D:** Both reactions follow the **Zone Phenomenon**. Optimal visible clumping occurs in the **Zone of Equivalence**. If there is an excess of antibody (Prozone) or antigen (Postzone), the lattice cannot form properly, leading to false-negative results. **3. High-Yield Clinical Pearls for NEET-PG:** * **Prozone Phenomenon:** Seen in Brucellosis and Secondary Syphilis; it can be overcome by serial dilution of the serum. * **Coombs Test:** An indirect/direct agglutination test used for Rh incompatibility and autoimmune hemolytic anemia. * **Passive Agglutination:** Converting a precipitation test into a more sensitive agglutination test by coating soluble antigens onto carrier particles like **Latex** (e.g., RA factor test, ASO test). * **Widal Test:** A standard tube agglutination test for Enteric fever.

Question 586: What are the most important cells involved in Type I hypersensitivity reactions?

A. Macrophages
B. Mast cells (Correct Answer)
C. Neutrophils
D. Lymphocytes

Explanation: **Explanation:** **Type I Hypersensitivity (Immediate Hypersensitivity)** is an IgE-mediated immune response. The hallmark of this reaction is the interaction between an allergen and **Mast cells** (and basophils). **Why Mast Cells are the correct answer:** Mast cells possess high-affinity receptors (**FcεRI**) for the Fc portion of IgE antibodies. Upon first exposure to an allergen, IgE is produced and "sensitizes" the mast cells by binding to these receptors. Upon re-exposure, the allergen cross-links the surface-bound IgE, triggering **degranulation**. This releases potent primary mediators like **histamine** and secondary mediators like leukotrienes and prostaglandins, leading to vasodilation, increased vascular permeability, and smooth muscle contraction. **Why other options are incorrect:** * **Macrophages (A):** Primarily involved in phagocytosis and antigen presentation. They play a role in Type IV (delayed) hypersensitivity but are not the primary effectors in Type I. * **Neutrophils (C):** These are the hallmark of acute inflammation and Type III hypersensitivity (Arthus reaction/Serum sickness), where they are recruited by immune complexes. * **Lymphocytes (D):** While B-lymphocytes produce the IgE and Th2 cells orchestrate the response, the "most important" effector cell that directly causes the clinical symptoms of Type I reactions is the Mast cell. **High-Yield Clinical Pearls for NEET-PG:** * **Preformed Mediator:** Histamine (responsible for immediate symptoms). * **Newly Synthesized Mediators:** Leukotrienes (C4, D4, E4) – these are 1000x more potent than histamine. * **Marker of Mast Cell Activation:** Serum **Tryptase** levels (used clinically to confirm anaphylaxis). * **Late-phase reaction:** Primarily mediated by **Eosinophils**, which are recruited by Eosinophilic Chemotactic Factor (ECF-A) released by mast cells.

Question 587: Which is the main cell involved in antibody-dependent cell-mediated cytotoxicity (ADCC)?

A. Natural killer cells (Correct Answer)
B. CD 4+ T cells
C. Cytotoxic T lymphocytes
D. B lymphocytes

Explanation: ### Explanation **Correct Option: A. Natural Killer (NK) cells** Antibody-dependent cell-mediated cytotoxicity (ADCC) is a mechanism of cell-mediated immune defense where an effector cell of the immune system actively lyses a target cell, whose membrane-surface antigens have been bound by specific antibodies. * **Mechanism:** NK cells express **CD16**, a low-affinity receptor for the Fc portion of IgG (**FcγRIII**). When IgG binds to a target cell (e.g., a virus-infected or tumor cell), the NK cell binds to the Fc region via CD16, triggering the release of **perforins and granzymes**, leading to apoptosis of the target cell. While macrophages, neutrophils, and eosinophils can also perform ADCC, **NK cells are the primary and most efficient mediators.** **Why Other Options are Incorrect:** * **B. CD4+ T cells:** These are Helper T cells that coordinate the immune response by secreting cytokines; they do not possess CD16 and do not participate in ADCC. * **C. Cytotoxic T lymphocytes (CTLs):** CTLs (CD8+) kill target cells via MHC-I restriction. They recognize antigens presented on MHC-I molecules, whereas ADCC is **MHC-independent**. * **D. B lymphocytes:** These are the cells responsible for producing antibodies (humoral immunity), not for the effector cytotoxic action of ADCC. **High-Yield Clinical Pearls for NEET-PG:** * **Marker for NK Cells:** CD16 (Fc receptor) and CD56. * **ADCC Mediators:** NK cells (Main), Macrophages, Monocytes, Neutrophils, and Eosinophils (specifically against helminths via IgE). * **Clinical Application:** Monoclonal antibodies used in cancer therapy (e.g., **Rituximab**) work largely by inducing ADCC via NK cells. * **Key Difference:** Unlike CTLs, NK cells do not require prior sensitization or MHC presentation to function.

Question 588: The Widal test is a type of:

A. Slide agglutination test
B. Tube agglutination test (Correct Answer)
C. Complement fixation test (CFT)
D. Ring precipitation test

Explanation: **Explanation:** The **Widal test** is a serological test used for the diagnosis of enteric fever (Typhoid and Paratyphoid). It is a classic example of a **Tube Agglutination Test**, specifically the **Felix-Widal test**. 1. **Why it is a Tube Agglutination Test:** In this method, serial dilutions of the patient's serum are mixed with standardized bacterial suspensions (O and H antigens of *Salmonella Typhi* and *S. Paratyphi*) in Dreyer’s tubes (for H antigen) or Felix tubes (for O antigen). This quantitative method allows for the determination of the **antibody titer**, which is crucial for distinguishing between a past infection/vaccination and a current active infection. 2. **Why other options are incorrect:** * **Slide Agglutination Test:** While a rapid slide Widal test exists for screening, the definitive, diagnostic Widal test referred to in standard textbooks and exams is the quantitative tube method. * **Complement Fixation Test (CFT):** This involves the consumption of complement by antigen-antibody complexes (e.g., Wassermann test for Syphilis). Widal relies on direct visible clumping (agglutination), not complement lysis. * **Ring Precipitation Test:** This is a precipitation reaction (e.g., Ascoli’s test) where a soluble antigen reacts with an antibody. Widal uses whole bacterial cells (particulate antigens), making it an agglutination reaction. **High-Yield Clinical Pearls for NEET-PG:** * **Antigens used:** ‘H’ (flagellar) and ‘O’ (somatic) antigens. * **Appearance:** ‘H’ agglutination is loose and cotton-woolly; ‘O’ agglutination is disc-like and granular. * **Timing:** Antibodies usually appear after the first week of fever. * **Interpretation:** A four-fold rise in titer between acute and convalescent sera is more diagnostic than a single high titer. * **False Positives:** Can occur in patients with chronic liver disease or prior TAB vaccination (Anamnestic response).

Question 589: Interleukin-2 (IL-2) is primarily produced by which type of cell?

A. T cells (Correct Answer)
B. B cells
C. Monocytes
D. Neutrophils

Explanation: **Explanation:** Interleukin-2 (IL-2), originally known as **T-cell growth factor**, is a critical cytokine in the adaptive immune response. It is primarily produced by **CD4+ T-helper (Th1) cells** and, to a lesser extent, by CD8+ T cells following activation by antigens and co-stimulatory signals. **Why T cells are the correct answer:** IL-2 acts in both an **autocrine** and **paracrine** fashion. Once secreted by activated T cells, it binds to IL-2 receptors (CD25) on the same or neighboring T cells. This binding triggers clonal expansion, differentiation into effector and memory cells, and the survival of Regulatory T cells (Tregs). It is the "master switch" for T-cell proliferation. **Why other options are incorrect:** * **B cells:** While B cells possess IL-2 receptors and respond to IL-2 by proliferating and secreting antibodies, they are not primary producers of this cytokine. * **Monocytes:** These cells primarily produce pro-inflammatory cytokines like **IL-1, IL-6, and TNF-alpha**, rather than IL-2. * **Neutrophils:** These are professional phagocytes involved in the innate immune response; they do not produce IL-2. **High-Yield Clinical Pearls for NEET-PG:** * **CD25:** This is the alpha chain of the IL-2 receptor. It is a marker for **Regulatory T cells (Tregs)** and activated T cells. * **Therapeutic Use:** Recombinant IL-2 (**Aldesleukin**) is used in the treatment of Metastatic Renal Cell Carcinoma and Melanoma. * **Immunosuppression:** Drugs like **Cyclosporine and Tacrolimus** work by inhibiting Calcineurin, which prevents the transcription of IL-2, thereby inhibiting T-cell activation. * **Basiliximab/Daclizumab:** These are monoclonal antibodies that act as **IL-2 receptor antagonists**, used to prevent acute organ transplant rejection.

Question 590: A patient presents with recurrent swelling of the lips. He has no itching and a positive family history. Which of the following is deficient in this patient?

A. C1, C2, C4
B. C1 inhibitor (Correct Answer)
C. C3b inactivator
D. C5-C8

Explanation: The clinical presentation of recurrent, non-pruritic swelling (angioedema) without urticaria (itching), coupled with a positive family history, is the classic triad for **Hereditary Angioedema (HAE)**. ### **Explanation of the Correct Answer** **Hereditary Angioedema** is caused by a deficiency or dysfunction of the **C1 esterase inhibitor (C1-INH)**. * **Mechanism:** C1-INH normally inhibits the classical complement pathway and the kinin system. Its deficiency leads to the uncontrolled activation of the kallikrein-kinin cascade, resulting in excessive production of **bradykinin**. * **Clinical Effect:** Bradykinin increases vascular permeability, leading to the characteristic episodic swelling of the face, lips, airway (life-threatening), and gastrointestinal tract. ### **Analysis of Incorrect Options** * **A. C1, C2, C4:** Deficiencies in early classical pathway components are strongly associated with **Systemic Lupus Erythematosus (SLE)** and other immune-complex diseases, as they are required for clearing apoptotic debris. * **C. C3b inactivator (Factor I):** Deficiency leads to the continuous consumption of C3. This results in low C3 levels and presents clinically as recurrent infections with **pyogenic bacteria** (e.g., *S. pneumoniae*). * **D. C5-C8:** Deficiencies in the Membrane Attack Complex (MAC) components (C5–C9) specifically predispose individuals to recurrent **Neisserial infections** (Meningitis and Gonorrhea). ### **NEET-PG High-Yield Pearls** * **Biochemical Marker:** The best screening test for HAE is a **low C4 level**, even between attacks. * **Treatment:** Acute attacks are treated with C1-INH concentrate or **Icatibant** (bradykinin B2 receptor antagonist). * **Contraindication:** Patients with HAE should avoid **ACE inhibitors**, as they prevent bradykinin breakdown and can trigger severe attacks.

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Immunology — MCQs

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