Immunopathology — MCQs

A 31-year-old man with AIDS complains of difficulty swallowing. Examination of his oral cavity demonstrates whitish membranes covering much of his tongue and palate. Endoscopy also reveals several whitish, ulcerated lesions in the esophagus. Which of the following enzymes converts the HIV genome into double-stranded DNA in host cells?

Q148Easy

HLA-B47 is associated with which of the following conditions?

Q149Easy

Biopsy of the parotid gland in Sjogren's syndrome typically shows infiltration by which type of inflammatory cell?

Q150Easy

MHC III codes for which of the following?

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 141: All of the following regarding acute graft rejection are true, except?

A. CD8+ T-cells directly destroy the graft.
B. It is the principal cause of early graft failure.
C. Preformed antibodies against graft are the main causative factor. (Correct Answer)
D. Cytokines secreted by CD4+ T-cells cause inflammation which destroys the graft.

Explanation: **Explanation:** The question asks for the **incorrect** statement regarding acute graft rejection. **1. Why Option C is the Correct Answer (The False Statement):** Preformed antibodies against the graft are the hallmark of **Hyperacute Rejection**, not acute rejection [1]. These antibodies (usually anti-ABO or anti-HLA) are present in the recipient's serum before transplantation, leading to immediate thrombosis and graft necrosis within minutes to hours [2]. In contrast, **Acute Rejection** is primarily a cell-mediated process occurring days to weeks after transplantation [1]. **2. Analysis of Other Options:** * **Option A (True):** Acute cellular rejection involves **Direct Pathway** activation where recipient CD8+ T-cells recognize donor MHC molecules and directly cause graft cell lysis (cytotoxicity) [4]. * **Option B (True):** Acute rejection is indeed the **principal cause of early graft failure** (typically occurring within the first few months), though it can also occur later if immunosuppression is reduced [1]. * **Option D (True):** CD4+ T-cells play a vital role by secreting cytokines (Delayed-Type Hypersensitivity), which recruit macrophages and promote inflammation, leading to graft tissue damage [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hyperacute Rejection:** Mediated by preformed antibodies; characterized by **fibrinoid necrosis** and "white graft" appearance [2]. * **Acute Rejection:** Primarily **T-cell mediated**. Histology shows **interstitial mononuclear cell infiltrates** and endothelitis (intimal inflammation) [1]. * **Chronic Rejection:** Occurs months to years later; characterized by **intimal thickening (arteriosclerosis)** and interstitial fibrosis. * **Graft-vs-Host Disease (GVHD):** Occurs when donor T-cells attack the recipient's tissues (common in bone marrow transplants); classic triad: Rash, Jaundice, and Diarrhea. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242. [3] 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. 180-181. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 240.

Question 142: Interleukin-6 is persistently raised in which of the following conditions?

A. Kawasaki disease
B. Viral encephalitis
C. HIV encephalitis
D. Behcet's disease (Correct Answer)

Explanation: **Explanation:** **Behcet’s Disease (Correct Answer):** Behcet’s disease is a chronic, multisystem inflammatory disorder characterized by a triad of oral ulcers, genital ulcers, and uveitis. The pathogenesis involves a profound dysregulation of the innate and adaptive immune systems. **Interleukin-6 (IL-6)** plays a pivotal role as a pro-inflammatory cytokine that drives the Th17 response and neutrophilic hyperactivity seen in this condition. Studies have consistently shown that IL-6 levels are **persistently elevated** in patients with Behcet’s disease, correlating with disease activity and the development of systemic manifestations like vasculitis and neuro-Behcet’s. **Why other options are incorrect:** * **Kawasaki Disease:** While IL-6 is elevated during the *acute* phase of this pediatric vasculitis, it typically normalizes once the febrile episode resolves or treatment (IVIG) is initiated [1]. It is not characterized by "persistent" elevation in a chronic sense. * **Viral Encephalitis:** This is an acute inflammatory process. Cytokine surges (including IL-6) occur rapidly but are transient, subsiding as the viral replication is controlled or the acute phase passes [2]. * **HIV Encephalitis:** While chronic inflammation exists in HIV, the cytokine profile is more complex, often involving TNF-alpha and IL-1. IL-6 may be elevated, but it is not the hallmark "persistent" biomarker specifically associated with the pathogenesis of HIV encephalitis in the same way it is for Behcet's. **High-Yield Clinical Pearls for NEET-PG:** * **Behcet’s Hallmark:** Look for the **Pathergy Test** (skin hyperreactivity to a minor needle prick) in clinical vignettes. * **HLA Association:** Strongly associated with **HLA-B51**. * **IL-6 Blockade:** Due to the persistent elevation of IL-6, **Tocilizumab** (an IL-6 receptor antagonist) is an emerging therapeutic option for refractory Behcet’s cases. * **Vessel Involvement:** Unlike many other vasculitides, Behcet’s can involve vessels of **all sizes** (small, medium, and large) on both the arterial and venous sides. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-100.

Question 143: What is the most common antibody found in Sjogren syndrome?

A. Anti-DNA topoisomerase
B. Anti-Centromere
C. Anti-RNA polymerase
D. Anti-Ribonucleoprotein (Correct Answer)

Explanation: **Explanation:** Sjögren syndrome is a chronic autoimmune disorder characterized by lymphocytic infiltration of exocrine glands, primarily the lacrimal and salivary glands. The diagnosis relies heavily on the presence of specific autoantibodies directed against **ribonucleoproteins (RNPs)** [1]. **1. Why the Correct Answer is Right:** The correct answer is **Anti-Ribonucleoprotein**. In Sjögren syndrome, the two hallmark antibodies are **SS-A (Ro)** and **SS-B (La)** [1]. Both of these are directed against small ribonucleoprotein particles. While they are not 100% specific (as they can appear in SLE), they are the most common and diagnostically significant antibodies for this condition. SS-A is found in 70-95% of cases, and SS-B is found in 60-90%. **2. Analysis of Incorrect Options:** * **A. Anti-DNA topoisomerase (Anti-Scl-70):** This is highly specific for **Diffuse Cutaneous Systemic Sclerosis**. * **B. Anti-Centromere:** This is the classic marker for **Limited Cutaneous Systemic Sclerosis (CREST syndrome)**. * **C. Anti-RNA polymerase III:** This is associated with **Diffuse Systemic Sclerosis** and indicates an increased risk for scleroderma renal crisis. **3. NEET-PG High-Yield Pearls:** * **Schirmer Test:** Used to quantify decreased lacrimation (objective evidence of keratoconjunctivitis sicca). * **Lip Biopsy:** The gold standard for diagnosis; it shows minor salivary gland involvement with focal lymphocytic aggregates (focus score). * **Malignancy Risk:** Patients with Sjögren syndrome have a **40-fold increased risk** of developing **B-cell MALT Lymphoma** (often presenting as persistent parotid swelling). * **Neonatal Lupus:** Pregnant women with Anti-Ro (SS-A) antibodies are at risk of having infants with congenital heart block. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 234-235.

Question 144: Which of the following is the WRONG combination regarding adhesion molecules and their corresponding CD markers?

A. VCAM - CD106
B. ICAM - CD102
C. ICAM1 - CD54
D. PECAM - CD64 (Correct Answer)

Explanation: This question tests your knowledge of **Adhesion Molecules**, which are critical for leukocyte trafficking and the inflammatory response. In the NEET-PG exam, matching Cluster of Differentiation (CD) markers to their common names is a high-yield topic. ### **Explanation of the Correct Answer** **Option D (PECAM - CD64) is the WRONG combination.** * **PECAM-1** (Platelet Endothelial Cell Adhesion Molecule-1) is actually **CD31**. It is expressed on leukocytes and endothelial cells and is primarily responsible for **diapedesis** (transmigration of leukocytes through the endothelial junction) [1]. * **CD64** is the marker for **FcγRI**, the high-affinity receptor for IgG found on macrophages, monocytes, and neutrophils. ### **Analysis of Other Options** * **A. VCAM - CD106:** Correct. Vascular Cell Adhesion Molecule-1 (VCAM-1) is CD106. It binds to VLA-4 integrins on leukocytes and is involved in firm adhesion. * **B. ICAM - CD102:** Correct. Intercellular Adhesion Molecule-2 (ICAM-2) is CD102. It is constitutively expressed on endothelial cells. * **C. ICAM-1 - CD54:** Correct. ICAM-1 is CD54. It is upregulated by cytokines (TNF, IL-1) and is the ligand for LFA-1 (CD11a/CD18) during firm adhesion. ### **High-Yield Clinical Pearls for NEET-PG** * **Selectins (Rolling):** L-Selectin (CD62L), E-Selectin (CD62E), P-Selectin (CD62P). * **Integrins (Adhesion):** LFA-1 (CD11a/CD18) and MAC-1 (CD11b/CD18). * **LAD Type 1:** Caused by a deficiency in **CD18** (integrin β2 chain), leading to impaired firm adhesion and recurrent infections without pus formation [1]. * **LAD Type 2:** Caused by a deficiency in **Sialyl-Lewis X** (ligand for selectins), leading to impaired rolling. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Question 145: TRALI is usually due to?

A. High titre anti-HLA antibodies in recipient plasma
B. Low titre anti-HLA antibodies in donor plasma
C. High titre anti-HLA antibodies in donor plasma (Correct Answer)
D. HPA-la on the platelet glycoprotein IIa receptor

Explanation: **Explanation:** **Transfusion-Related Acute Lung Injury (TRALI)** is a life-threatening complication of blood transfusion characterized by acute respiratory distress and non-cardiogenic pulmonary edema. **1. Why Option C is Correct:** The most widely accepted mechanism for TRALI is the **"Two-Hit Hypothesis."** The "second hit" is typically the infusion of **high-titre anti-HLA (Human Leukocyte Antigen)** or anti-neutrophil antibodies present in the **donor's plasma**. These antibodies react against the recipient’s white blood cells (neutrophils) that have already been "primed" (the first hit) by an underlying clinical condition like sepsis or trauma. This interaction causes neutrophils to sequester in the pulmonary microvasculature, releasing reactive oxygen species and enzymes that damage the alveolar-capillary membrane, leading to fluid leakage into the lungs. **2. Why the Other Options are Incorrect:** * **Option A:** TRALI is mediated by antibodies in the **donor** plasma attacking the recipient's cells, not the other way around. * **Option B:** Low titres are generally insufficient to trigger the massive inflammatory cascade required for TRALI; high-titre antibodies are the classic culprit. * **Option D:** HPA-1a antibodies are associated with **Neonatal Alloimmune Thrombocytopenia (NAIT)** or **Post-Transfusion Purpura (PTP)**, not TRALI. **Clinical Pearls for NEET-PG:** * **Most common cause of transfusion-related fatalities** reported to the FDA. * **Risk Factors:** Multiparous women are the most common donors of implicated plasma (due to sensitization during pregnancy). * **Clinical Presentation:** Sudden onset (within 6 hours of transfusion) of dyspnea, hypoxia, and bilateral infiltrates on CXR, often with **hypotension** (unlike TACO, which presents with hypertension). * **Management:** Immediate cessation of transfusion and aggressive respiratory support. Diuretics are generally avoided as the patient is often hypovolemic.

Question 146: Acute graft-versus-host-disease (GVHD) commonly involves all of the following organs, except:

A. Brain (Correct Answer)
B. Skin
C. Liver
D. Small & large intestines

Explanation: **Explanation:** Acute Graft-versus-Host Disease (GVHD) occurs when immunocompetent donor T-cells recognize the recipient's HLA antigens as foreign and mount an immune attack [1]. This typically occurs within 100 days of a hematopoietic stem cell transplant. **Why Brain is the Correct Answer:** The **Brain (Option A)** is not a primary target in acute GVHD. The central nervous system is considered an "immune-privileged" site, protected by the blood-brain barrier, and lacks the specific epithelial targets typically attacked by donor T-cells in the acute phase. **Why the other options are incorrect:** Acute GVHD classically targets three main organ systems characterized by high cell turnover or specific cytokine environments: * **Skin (Option B):** The most common and usually the first organ involved. It presents as a maculopapular rash, often starting on the palms, soles, and neck, which can progress to generalized erythroderma or toxic epidermal necrolysis-like lesions [1]. * **Liver (Option C):** Involvement manifests as cholestatic jaundice due to damage to the small bile ducts, leading to elevated bilirubin and alkaline phosphatase [1]. * **Small & Large Intestines (Option D):** The GI tract is a major target. Damage to the mucosal epithelium results in profuse, watery, or bloody diarrhea, abdominal pain, and ileus [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Donor CD4+ and CD8+ T-cells are the primary effectors. * **Histology:** Look for **"Satellite cell necrosis"** (lymphocytes adjacent to apoptotic keratinocytes) in skin biopsies [1]. * **Chronic GVHD:** Occurs after 100 days and mimics autoimmune diseases like Systemic Sclerosis (Scleroderma) or Sjögren’s syndrome. * **Prophylaxis:** Methotrexate and Cyclosporine are commonly used to inhibit T-cell activation. **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. 182-183.

Question 147: A 31-year-old man with AIDS complains of difficulty swallowing. Examination of his oral cavity demonstrates whitish membranes covering much of his tongue and palate. Endoscopy also reveals several whitish, ulcerated lesions in the esophagus. Which of the following enzymes converts the HIV genome into double-stranded DNA in host cells?

A. DNA polymerase (Pol-1)
B. DNA polymerase (Pol-2)
C. Integrase
D. Reverse transcriptase (Correct Answer)

Explanation: The clinical presentation of a patient with AIDS presenting with oral thrush (candidiasis) and esophageal ulcers is highly suggestive of advanced immunosuppression. The question focuses on the replication cycle of the **Human Immunodeficiency Virus (HIV)**, a retrovirus. **1. Why Reverse Transcriptase is Correct:** HIV is an RNA virus. Upon entering the host cell (CD4+ T cell), its single-stranded RNA genome must be converted into double-stranded DNA (dsDNA) to be integrated into the host genome [1]. This process is catalyzed by the enzyme **Reverse Transcriptase (RNA-dependent DNA polymerase)**. This enzyme lacks proofreading capabilities, leading to the high mutation rate characteristic of HIV. **2. Why the Other Options are Incorrect:** * **DNA Polymerase (Pol-1 & Pol-2):** These are host cell enzymes involved in eukaryotic DNA replication and repair. They synthesize DNA from a DNA template, not from the viral RNA template. * **Integrase:** This viral enzyme is responsible for inserting (integrating) the newly synthesized viral dsDNA into the host cell's nuclear DNA [1]. It acts *after* reverse transcriptase has completed its job. **Clinical Pearls for NEET-PG:** * **HIV Genes:** * *gag:* Codes for structural proteins (p24 capsid). * *pol:* Codes for enzymes (**Reverse Transcriptase, Integrase, Protease**). * *env:* Codes for envelope glycoproteins (gp120 for attachment, gp41 for fusion). * **Diagnostic Marker:** p24 antigen is the earliest detectable protein in the blood during the window period. * **Opportunistic Infection:** Esophageal candidiasis is an **AIDS-defining illness**, typically occurring when the CD4 count falls below 100 cells/mm³. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 255-256.

Question 148: HLA-B47 is associated with which of the following conditions?

A. Myasthenia gravis
B. Behcet's disease
C. Congenital adrenal hyperplasia (Correct Answer)
D. Abacavir hypersensitivity

Explanation: **Explanation:** The correct answer is **Congenital Adrenal Hyperplasia (CAH)**. The association between HLA (Human Leukocyte Antigen) alleles and specific diseases is a high-yield topic in immunopathology. **HLA-B47** is specifically linked to 21-hydroxylase deficiency, the most common cause of Congenital Adrenal Hyperplasia [1]. This association occurs because the gene encoding the 21-hydroxylase enzyme (*CYP21A2*) is located within the Major Histocompatibility Complex (MHC) locus on Chromosome 6, leading to strong linkage disequilibrium between the HLA-B47 allele and the defective enzyme gene. **Analysis of Incorrect Options:** * **A. Myasthenia gravis:** This autoimmune neuromuscular disorder is most commonly associated with **HLA-DR3** and **HLA-B8**. * **B. Behcet’s disease:** This systemic vasculitis has a very strong and classic association with **HLA-B51**. * **C. Abacavir hypersensitivity:** A critical pharmacogenetic association exists between the antiretroviral drug abacavir and **HLA-B*57:01**. Testing for this allele is mandatory before starting the drug to prevent life-threatening hypersensitivity reactions. **High-Yield Clinical Pearls for NEET-PG:** * **HLA-B27:** Associated with Seronegative Spondyloarthropathies (Ankylosing spondylitis, Reiter’s syndrome, Psoriatic arthritis, Enteropathic arthritis). * **HLA-DR3/DR4:** Associated with Type 1 Diabetes Mellitus. * **HLA-DQ2/DQ8:** Associated with Celiac disease. * **HLA-DR2:** Associated with Multiple Sclerosis and Goodpasture syndrome. * **HLA-DR4:** Associated with Rheumatoid Arthritis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1130-1133.

Question 149: Biopsy of the parotid gland in Sjogren's syndrome typically shows infiltration by which type of inflammatory cell?

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

Explanation: **Explanation:** **Sjögren’s Syndrome** is a chronic autoimmune disorder characterized by immune-mediated destruction of the exocrine glands, primarily the lacrimal and salivary glands [1]. **Why Lymphocytes are the correct answer:** The hallmark histopathological feature of Sjögren’s syndrome is **focal lymphocytic infiltration** of the glandular parenchyma [1]. These infiltrates are predominantly composed of **CD4+ T-helper cells** and some B cells [1]. In the parotid or minor salivary glands, these lymphocytes replace the normal acini, eventually leading to the formation of **epimyoepithelial islands**. This chronic inflammatory process results in glandular atrophy and fibrosis, manifesting clinically as xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes) [1]. **Why other options are incorrect:** * **Neutrophils:** These are markers of acute bacterial inflammation or abscess formation [3]. Sjögren’s is a chronic autoimmune process, not an acute infection. * **Eosinophils:** These are typically associated with Type I hypersensitivity (allergic) reactions, parasitic infections, or specific conditions like Kimura disease [3]. * **Basophils:** These are rarely seen in tissue biopsies and are generally involved in systemic allergic responses or myeloproliferative disorders. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Gold Standard:** Lip biopsy (minor salivary gland biopsy) showing $\ge$ 1 focus of 50+ lymphocytes per 4 $mm^2$. * **Serology:** Positive for **Anti-Ro (SS-A)** and **Anti-La (SS-B)** antibodies [1]. * **Increased Risk:** Patients have a 40-fold increased risk of developing **B-cell Non-Hodgkin Lymphoma** (specifically MALT lymphoma) [2]. * **Schirmer’s Test:** Used to quantify decreased tear production. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 234-235. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 236. [3] 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 150: MHC III codes for which of the following?

A. TNF alpha (Correct Answer)
B. IL 1
C. HLA A
D. HLA B

Explanation: The Major Histocompatibility Complex (MHC) is a cluster of genes located on the **short arm of Chromosome 6**. While MHC I and II are primarily involved in antigen presentation, MHC III is a diverse region coding for various immune-related proteins. ### **Explanation of the Correct Answer** **Option A (TNF-alpha)** is correct. The MHC Class III region does not encode cell-surface molecules for antigen presentation [1]. Instead, it codes for several soluble proteins involved in the inflammatory response and the complement system. Key products include: * **Cytokines:** Tumor Necrosis Factor (TNF-α) and Lymphotoxin (TNF-β). * **Complement components:** C2, C4 (C4A and C4B), and Factor B. * **Heat Shock Proteins:** HSP70. ### **Explanation of Incorrect Options** * **Option B (IL-1):** Interleukin-1 is a pro-inflammatory cytokine primarily produced by macrophages. It is encoded by genes on **Chromosome 2**, not within the MHC locus. * **Options C and D (HLA A and HLA B):** These are **MHC Class I** molecules. MHC Class I includes HLA-A, HLA-B, and HLA-C, which are expressed on all nucleated cells and present endogenous antigens to CD8+ T-cells [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **MHC Location:** Short arm of Chromosome 6 (6p) [1]. * **MHC Class I:** HLA-A, B, C (presents to CD8+ T cells). * **MHC Class II:** HLA-DP, DQ, DR (presents to CD4+ T cells). * **MHC Class III:** Unique because it **does not** code for HLA molecules or participate in antigen presentation. * **Rule of 8:** MHC I × CD8 = 8; MHC II × CD4 = 8. This helps remember which T-cell interacts with which MHC class. **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.

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