Immunopathology — MCQs

An 8-year-old boy presents with periorbital edema and throbbing headaches. His parents report that the boy had a 'strep throat' 2 weeks ago. Urinalysis shows 3+ hematuria. A renal biopsy shows hypercellular glomeruli, and electron microscopic examination of glomeruli discloses subepithelial 'humps.' Which of the following best explains the pathogenesis of glomerulonephritis in this patient?

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 181: Idiopathic thrombocytopenic purpura is due to which type of hypersensitivity?

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

Explanation: **Explanation:** **Why Type II Hypersensitivity is Correct:** Immune Thrombocytopenic Purpura (ITP) is a classic example of **Type II (Antibody-mediated) Hypersensitivity** [1]. In this condition, the body produces autoantibodies (usually IgG) directed against specific self-antigens on the platelet surface, most commonly the **Glycoprotein IIb/IIIa (GP IIb/IIIa)** or **GP Ib/IX** complex. Once coated with these antibodies (opsonization), the platelets are recognized by the Fc receptors on splenic macrophages and prematurely destroyed in the spleen, leading to thrombocytopenia [2]. **Why Other Options are Incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). ITP does not involve IgE or allergen triggers. * **Type III (Immune-complex):** Caused by the deposition of soluble antigen-antibody complexes in tissues (e.g., SLE, Post-streptococcal glomerulonephritis). In ITP, the antibody binds to a fixed antigen on a cell surface, not a soluble one. * **Type IV (Delayed):** Cell-mediated immunity involving T-lymphocytes (e.g., Mantoux test, Contact dermatitis). ITP is primarily an antibody-driven process. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Destruction:** Extravascular hemolysis/destruction occurring primarily in the **Spleen** [3]. * **Bone Marrow Finding:** Characterized by an **increased number of Megakaryocytes** (compensatory response to peripheral destruction) [3]. * **Clinical Presentation:** Petechiae, purpura, and mucosal bleeding (epistaxis, menorrhagia) with a normal coagulation profile (PT/aPTT) but prolonged bleeding time [2], [3]. * **Treatment Tip:** Splenectomy is effective because it removes both the site of antibody production and the site of platelet destruction [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 651-652. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-667.

Question 182: Which of the following cells are defective in chronic granulomatous disease?

A. Neutrophils (Correct Answer)
B. Lymphocytes
C. Plasma cells
D. Killer T cells

Explanation: **Explanation:** **Chronic Granulomatous Disease (CGD)** is a primary immunodeficiency disorder caused by a genetic defect in the **NADPH oxidase enzyme complex**. This enzyme is responsible for the "respiratory burst" in phagocytes, which produces reactive oxygen species (ROS) like superoxide radicals to kill ingested microorganisms. 1. **Why Neutrophils are correct:** Neutrophils (and macrophages) are the primary professional phagocytes. In CGD, these cells can ingest bacteria but cannot produce the superoxide required to kill them [1]. This leads to the formation of persistent granulomas [2] as the body attempts to wall off the surviving intracellular pathogens. 2. **Why other options are incorrect:** * **Lymphocytes (B and T cells):** These are involved in adaptive immunity (antibody production and cell-mediated killing). CGD is a defect of the innate immune system's phagocytic function, not adaptive recognition. * **Plasma cells:** These are differentiated B cells that produce antibodies. Humoral immunity is typically intact in CGD patients. * **Killer T cells (CD8+):** These cells destroy virally infected or tumor cells via perforins and granzymes, a pathway independent of the NADPH oxidase system. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most commonly **X-linked recessive** (defect in the *gp91phox* subunit). * **Pathogens:** Patients are highly susceptible to **Catalase-positive organisms** (e.g., *Staphylococcus aureus*, *Aspergillus*, *Nocardia*, *Serratia marcescens*). These organisms neutralize their own H2O2, leaving the defective neutrophil with no oxidative means to kill them. * **Diagnosis:** The gold standard is the **Dihydrorhodamine (DHR) 123 flow cytometry test** (more sensitive). The classic test is the **Nitroblue Tetrazolium (NBT) dye test**, which remains colorless (negative) in CGD patients. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 89-91. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 195-196.

Question 183: Which of the following antigen-presenting cells does not express MHC Class II molecules?

A. Follicular cells of the thyroid (Correct Answer)
B. Microglia of the brain
C. Langerhans cells of the skin
D. Dendritic cells of lymphoid tissues

Explanation: ### Explanation The expression of **MHC Class II molecules** is the hallmark of **Professional Antigen-Presenting Cells (APCs)**. These molecules are essential for presenting exogenous antigens to CD4+ T-helper cells. **Why Follicular cells of the thyroid is the correct answer:** Under normal physiological conditions, **thyroid follicular cells** are non-professional APCs and **do not express MHC Class II** [1]. They only express MHC Class I (found on all nucleated cells) [1]. However, in autoimmune states like **Hashimoto’s thyroiditis** or Graves' disease, these cells can be induced to express MHC II by cytokines like Interferon-gamma (IFN-̳), but they are not constitutive expressors [1]. **Analysis of Incorrect Options:** * **Microglia of the brain:** These are the resident macrophages of the Central Nervous System (CNS). As part of the mononuclear phagocyte system, they constitutively express MHC II to initiate immune responses within the brain. * **Langerhans cells of the skin:** These are specialized dendritic cells located in the stratum spinosum of the epidermis [2]. They are highly efficient professional APCs that capture cutaneous antigens and migrate to lymph nodes [2]. * **Dendritic cells (DCs) of lymphoid tissues:** DCs are considered the **most potent professional APCs** [1]. They constitutively express high levels of MHC II and co-stimulatory molecules (B7-1, B7-2) required for naive T-cell activation. **High-Yield Clinical Pearls for NEET-PG:** * **Professional APCs include:** Dendritic cells (most potent), Macrophages, and B-cells [1]. * **MHC Class II** is encoded by the **HLA-D region** (DP, DQ, DR) on Chromosome 6. * **Invariant chain (Ii):** A protein that binds to the MHC II groove in the ER to prevent premature binding of self-peptides. * **Non-professional APCs:** Include vascular endothelial cells and fibroblasts, which express MHC II only when stimulated by IFN-̳. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 156-157. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 174-175.

Question 184: NADPH oxidase deficiency causes which of the following conditions?

A. Chédiak-Higashi syndrome
B. Chronic granulomatous disease (Correct Answer)
C. Leukocyte adhesion defect type 1
D. Leukocyte adhesion defect type 2

Explanation: **Explanation:** **Correct Answer: B. Chronic Granulomatous Disease (CGD)** Chronic Granulomatous Disease is caused by a genetic deficiency in the **NADPH oxidase enzyme complex** (most commonly the gp91phox subunit, which is X-linked). This enzyme is responsible for the "respiratory burst," converting molecular oxygen into superoxide radicals ($O_2^-$). Without NADPH oxidase, phagocytes cannot generate reactive oxygen species (ROS) like H₂O₂ and HOCl (hypochlorite) to kill ingested microbes. Consequently, macrophages wall off the surviving bacteria, leading to the formation of **granulomas** throughout the body. **Analysis of Incorrect Options:** * **A. Chédiak-Higashi syndrome:** This is a defect in **lysosomal trafficking (LYST gene)**, leading to impaired fusion of phagosomes with lysosomes [1]. It is characterized by giant cytoplasmic granules in neutrophils [1]. * **C. Leukocyte Adhesion Defect (LAD) Type 1:** Caused by a deficiency of **CD18 (β2 integrins)**. It results in the inability of leukocytes to adhere to the endothelium and migrate into tissues. * **D. Leukocyte Adhesion Defect (LAD) Type 2:** Caused by a deficiency of **Sialyl-Lewis X**, leading to a defect in the "rolling" phase of leukocyte recruitment. **High-Yield Clinical Pearls for NEET-PG:** * **Catalase-positive organisms:** Patients with CGD are specifically susceptible to organisms like *Staphylococcus aureus*, *Aspergillus*, *Serratia marcescens*, and *Nocardia*. These bacteria neutralize their own H₂O₂, leaving the host cell with no ROS for killing. * **Diagnostic Test:** The gold standard is the **Dihydrorhodamine (DHR) 123 flow cytometry test** (shows decreased fluorescence). The older **Nitroblue Tetrazolium (NBT) dye test** remains a classic exam favorite (CGD cells fail to turn blue). * **Inheritance:** Most common is **X-linked recessive**, though autosomal recessive forms exist. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.

Question 185: Steven Johnson Syndrome is seen with what kind of hypersensitivity reaction?

A. Type 1
B. Type 2
C. Type 3
D. Type 4 (Correct Answer)

Explanation: **Explanation:** **Correct Option: D (Type 4 Hypersensitivity)** Stevens-Johnson Syndrome (SJS) and its more severe variant, Toxic Epidermal Necrolysis (TEN), are classic examples of **Type 4 (Delayed-type) Hypersensitivity reactions**, specifically **Type IVc** [1]. The reaction is mediated by **cytotoxic T-cells (CD8+)** and Natural Killer (NK) cells. Upon exposure to a trigger (usually drugs like sulfonamides, anticonvulsants, or NSAIDs), these T-cells release cytotoxic molecules such as **Granulysin**, Perforin, and Granzyme B. This leads to widespread apoptosis of keratinocytes, resulting in the characteristic epidermal detachment and mucosal erosions. **Why other options are incorrect:** * **Type 1 (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Urticaria) [2]. SJS does not involve immediate IgE-mediated responses. * **Type 2 (Antibody-mediated):** Involves IgG/IgM antibodies directed against cell surface antigens (e.g., Pemphigus Vulgaris, Goodpasture syndrome) [2]. SJS is T-cell mediated, not antibody-mediated. * **Type 3 (Immune-complex):** Caused by deposition of antigen-antibody complexes (e.g., SLE, Serum Sickness). While some drug reactions are Type 3, SJS specifically involves direct cellular cytotoxicity. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of 10":** SJS involves <10% body surface area (BSA) skin detachment; SJS/TEN overlap is 10–30%; TEN is >30%. * **Key Mediator:** **Granulysin** is the most specific marker for keratinocyte death in SJS/TEN. * **Genetic Association:** HLA-B*1502 (associated with Carbamazepine use in Asians) and HLA-B*5801 (Allopurinol). * **Nikolsky Sign:** Positive (the top layer of skin slips away from the lower layers when rubbed). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 173-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 186: What does autologous transplant refer to?

A. Graft from an individual of the same genetic constitution
B. Graft from oneself (Correct Answer)
C. Graft from twins
D. Graft from a member of a different species

Explanation: **Explanation:** In immunopathology, transplants are classified based on the genetic relationship between the donor and the recipient. **1. Why the Correct Answer is Right:** An **Autologous transplant (Autograft)** refers to a graft where the donor and the recipient are the **same individual**. Since the tissue is genetically identical to the host, there is no immune response, and the risk of graft rejection is zero. * *Clinical Examples:* Skin grafting for burns, bone marrow harvesting before high-dose chemotherapy, and using the saphenous vein for coronary artery bypass grafting (CABG). **2. Analysis of Incorrect Options:** * **Option A & C (Isograft/Syngeneic graft):** These refer to grafts between individuals of the **same genetic constitution**, which occurs only in **monozygotic (identical) twins** [1]. While rejection is also absent here, the term "autologous" specifically implies self-to-self. * **Option D (Xenograft):** This refers to a graft between members of **different species** (e.g., a porcine/pig heart valve transplanted into a human) [1]. These are subject to vigorous hyperacute or acute rejection. * **Allograft (not listed):** This is the most common type, referring to a graft between genetically different members of the **same species** [1] (e.g., kidney transplant from a non-twin sibling or deceased donor). **NEET-PG High-Yield Pearls:** * **Order of Rejection Risk:** Xenograft > Allograft > Isograft = Autograft. * **MHC/HLA:** Rejection in allografts is primarily mediated by T-cell recognition of non-self **MHC (Major Histocompatibility Complex)** molecules [1]. * **Graft vs. Host Disease (GVHD):** This occurs most commonly in allogeneic bone marrow transplants where the donor's T-cells attack the recipient's tissues. It **cannot** occur in autologous transplants. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-240.

Question 187: Anaphylactic shock is caused by which type of hypersensitivity reaction?

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

Explanation: **Explanation:** **Type I Hypersensitivity (Immediate Hypersensitivity)** is the correct answer [1]. Anaphylactic shock is the most severe, systemic form of this reaction [4]. It occurs when an allergen (e.g., penicillin, bee sting, peanuts) cross-links **IgE antibodies** already bound to the surface of **mast cells and basophils** in a previously sensitized individual [2]. This triggers immediate degranulation and the release of vasoactive amines like **histamine**, leading to systemic vasodilation, increased vascular permeability, and bronchoconstriction [3]. **Why other options are incorrect:** * **Type II (Antibody-mediated):** Involves IgG or IgM antibodies directed against antigens on specific cell surfaces or tissues (e.g., Autoimmune Hemolytic Anemia, Myasthenia Gravis) [1]. * **Type III (Immune complex-mediated):** Caused by the deposition of antigen-antibody complexes in tissues, leading to complement activation and inflammation (e.g., SLE, Post-streptococcal Glomerulonephritis, Arthus reaction). * **Type IV (Delayed-type):** A T-cell mediated response (not antibody-mediated) that takes 24–72 hours to develop (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Key Mediator:** Histamine is the primary mediator; however, **Leukotrienes (C4, D4, E4)** are the most potent bronchoconstrictors [3]. * **Drug of Choice:** Epinephrine (Adrenaline) 1:1000 IM is the immediate treatment for anaphylaxis. * **Biomarker:** Serum **Tryptase** levels are measured to confirm a diagnosis of anaphylaxis post-event. * **Mnemonic (ACID):** **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed (IV). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213.

Question 188: In patients with myasthenia gravis, the characteristic autoantibody is directed against which of the following?

A. Acetylcholine
B. Acetylcholine receptors (Correct Answer)
C. Acetylcholine vesicles in the nerve terminal
D. Actin-myosin complex of the muscle

Explanation: **Explanation:** **Myasthenia Gravis (MG)** is a classic example of a **Type II Hypersensitivity reaction** [1]. The pathophysiology involves the production of autoantibodies that target the **postsynaptic nicotinic acetylcholine receptors (AChR)** at the neuromuscular junction (NMJ) [1], [2]. These antibodies cause receptor degradation, blockade of the binding site, and complement-mediated damage to the postsynaptic membrane, leading to muscle weakness and fatigability [1]. **Analysis of Options:** * **Option B (Correct):** The primary target in ~85% of MG patients is the **ACh receptor** [2]. In seronegative cases, antibodies against **MuSK** (Muscle-Specific Kinase) or **LRP4** are often found. * **Option A:** Antibodies are directed against the *receptor*, not the neurotransmitter (Acetylcholine) itself [1]. * **Option C:** This describes the site of pathology for **Lambert-Eaton Myasthenic Syndrome (LEMS)**, where antibodies target **P/Q-type voltage-gated calcium channels**, preventing the release of acetylcholine vesicles. * **Option D:** Actin and myosin are intracellular contractile proteins. While anti-striated muscle antibodies (anti-titin) can be seen in MG (especially with thymoma), they are not the primary diagnostic autoantibody. **High-Yield Clinical Pearls for NEET-PG:** * **Thymic Association:** 65-70% of patients have **thymic hyperplasia**, and 10-15% have a **thymoma**. * **Clinical Hallmark:** Fluctuating muscle weakness that worsens with activity and improves with rest (Diurnal variation) [1], [2]. * **Diagnosis:** **Edrophonium (Tensilon) test** (rapid improvement) or repetitive nerve stimulation (decremental response). * **Treatment:** Acetylcholinesterase inhibitors (Pyridostigmine) are the first-line symptomatic treatment. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238.

Question 189: Lupus anticoagulants may cause all of the following except?

A. Recurrent abortion
B. False positive VDRL results
C. Increased prothrombin time
D. None of the above (Correct Answer)

Explanation: **Explanation:** Lupus Anticoagulant (LA) is a type of antiphospholipid antibody (aPL) found in patients with Systemic Lupus Erythematosus (SLE) or Antiphospholipid Syndrome (APS). Despite its name, it is a **pro-thrombotic** agent *in vivo* [1]. **1. Why "None of the above" is correct:** All the listed options (A, B, and C) are recognized clinical or laboratory manifestations of Lupus Anticoagulant. Therefore, none of them can be excluded. **2. Analysis of Options:** * **Recurrent Abortion (Option A):** LA causes thrombosis in the placental vessels, leading to placental insufficiency, fetal loss, and recurrent spontaneous abortions [1]. This is a hallmark of Antiphospholipid Syndrome. * **False Positive VDRL (Option B):** The VDRL/RPR tests for syphilis use cardiolipin as an antigen. Since LA is an antiphospholipid antibody, it cross-reacts with the test reagent, leading to a biological false-positive result for syphilis [2]. * **Increased Prothrombin Time (Option C):** This is the "laboratory paradox." Although LA causes clotting in the body, it interferes with phospholipid-dependent coagulation tests *in vitro*. While it most classically prolongs the **Activated Partial Thromboplastin Time (aPTT)**, it can also prolong the **Prothrombin Time (PT)** and the Dilute Russell Viper Venom Time (dRVVT) by interfering with the assembly of coagulation factor complexes on the phospholipid surface [1]. **Clinical Pearls for NEET-PG:** * **The Paradox:** LA causes **thrombosis** (in vivo) but **prolonged clotting times** (in vitro) [1]. * **Mixing Study:** If aPTT is prolonged due to LA, it will **not correct** upon mixing with normal plasma (unlike factor deficiencies). * **Most Specific Test:** The **dRVVT** is considered the most specific screening test for Lupus Anticoagulant. * **Diagnostic Criteria:** Diagnosis of APS requires one clinical criteria (thrombosis or pregnancy loss) and one laboratory criteria (LA, anti-cardiolipin, or anti-β2-glycoprotein I antibodies) positive on two occasions 12 weeks apart [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 626-627. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 134-135.

Question 190: An 8-year-old boy presents with periorbital edema and throbbing headaches. His parents report that the boy had a 'strep throat' 2 weeks ago. Urinalysis shows 3+ hematuria. A renal biopsy shows hypercellular glomeruli, and electron microscopic examination of glomeruli discloses subepithelial 'humps.' Which of the following best explains the pathogenesis of glomerulonephritis in this patient?

A. Antineutrophil cytoplasmic autoantibodies
B. Deposition of circulating immune complexes (Correct Answer)
C. Directly cytotoxic IgG and IgM antibodies
D. IgE-mediated mast cell degranulation

Explanation: ### Explanation The clinical presentation of an 8-year-old boy with periorbital edema, hematuria, and a recent history of "strep throat" (2 weeks prior) is classic for **Post-Streptococcal Glomerulonephritis (PSGN)** [1]. **1. Why the Correct Answer is Right:** PSGN is a **Type III Hypersensitivity reaction**. It is caused by the **deposition of circulating immune complexes** (antigen-antibody complexes) within the glomerular basement membrane [1]. These complexes (specifically involving streptococcal antigens like SpeB) activate the classical complement pathway, leading to neutrophil recruitment and glomerular inflammation. The characteristic electron microscopy finding of **subepithelial "humps"** represents these large immune deposits sitting between the epithelial cells (podocytes) and the basement membrane [1]. **2. Why the Incorrect Options are Wrong:** * **Option A:** Antineutrophil cytoplasmic autoantibodies (ANCA) are associated with Pauci-immune glomerulonephritis (e.g., Granulomatosis with polyangiitis), which typically lacks significant immune deposits. * **Option C:** Directly cytotoxic antibodies (Type II Hypersensitivity) are seen in **Goodpasture Syndrome**, where antibodies target the glomerular basement membrane directly, showing a linear (not granular) pattern on immunofluorescence [1]. * **Option D:** IgE-mediated degranulation (Type I Hypersensitivity) is involved in allergic reactions and asthma, not the pathogenesis of post-infectious glomerulonephritis. **3. NEET-PG High-Yield Pearls:** * **Latent Period:** Typically 1–3 weeks after pharyngitis or 3–6 weeks after pyoderma (impetigo) [1]. * **Light Microscopy:** Diffuse hypercellularity (due to leukocyte infiltration and mesangial proliferation) [1]. * **Immunofluorescence:** "Starry sky" or "lumpy-bumpy" appearance due to granular IgG and C3 deposits [1]. * **Serology:** Low C3 levels (due to consumption) and elevated ASO (Anti-Streptolysin O) or Anti-DNase B titers. * **Prognosis:** Excellent in children; most recover spontaneously with conservative management. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-915.

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Transplantation Immunopathology

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Immune Response to Infections

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