Immunopathology Practice Questions

Q: A 40-year-old man presents with yellow skin and sclerae, abdominal tenderness, and dark urine. Physical examination reveals jaundice and mild hepatomegaly. Laboratory studies show elevated serum bilirubin (3.1 mg/dL), decreased serum albumin (2.5 g/dL), and prolonged prothrombin time (17 seconds). Serologic tests reveal antibodies to hepatitis B core antigen (IgG anti-HBcAg). The serum is also positive for HBsAg and HBeAg. What glycoprotein on virally infected hepatocytes provides a target for cell-mediated cytotoxicity in this patient?

Class I HLA molecules. The clinical presentation and serology (HBsAg+, HBeAg+, IgG anti-HBcAg) indicate **Chronic Active Hepatitis B**. In viral hepatitis, the liver injury is not caused by the virus itself (HBV is not cytopathic) but by the host’s immune response against infected hepatocytes [1]. **1. Why Class I HLA is correct:** Cytotoxic T Lymphocytes (CTLs), which are **CD8+ T cells**, are the primary effectors of cell-mediated immunity against viral infections. For a CTL to recognize and kill a virally infected cell, the viral antigens must be processed and presented on the cell surface in association with **Class I HLA molecules (HLA-A, B, or C)**. This "MHC restriction" ensures that CD8+ cells specifically target intracellular pathogens. The TCR (T-cell receptor) on the CD8+ cell binds the HLA I-antigen complex, leading to hepatocyte apoptosis via perforins and granzymes. **2. Why incorrect options are wrong:** * **CD4:** This is a surface marker for Helper T cells, which recognize antigens presented by Class II HLA molecules. They coordinate the immune response but do not directly provide the "target" for cytotoxicity. * **CD8:** This is the marker on the effector T cell (the "attacker"), not the glycoprotein on the target hepatocyte. * **Class II HLA molecules:** These are primarily expressed on professional antigen-presenting cells (APCs) like macrophages and B cells, not on hepatocytes. They present exogenous antigens to CD4+ Helper T cells. **Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD8+ = MHC I; CD4+ = MHC II (Rule of 8: 8\u00D71=8; 4\u00D72=8). * **HBV Pathogenesis:** The "ground-glass" appearance of hepatocytes in chronic HBV is due to the accumulation of HBsAg in the endoplasmic reticulum [1]. * **HBeAg:** Its presence signifies high viral replication and high infectivity [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 838-845.

Q: Which of the following is NOT a pro-inflammatory cytokine?

IL-10. ### Explanation The inflammatory response is tightly regulated by a balance between **pro-inflammatory** and **anti-inflammatory** cytokines [1]. **Why IL-10 is the correct answer:** **IL-10** is a potent **anti-inflammatory cytokine**. Its primary role is to terminate the inflammatory response and prevent tissue damage caused by overactive immunity. It achieves this by: * Inhibiting the synthesis of pro-inflammatory cytokines (like IL-1, IL-6, and TNF). * Downregulating the expression of MHC Class II and co-stimulatory molecules on macrophages and dendritic cells. * Inhibiting the "oxidative burst" in macrophages. **Why the other options are incorrect:** * **IL-1:** A classic pro-inflammatory cytokine produced by macrophages [1]. It induces fever (endogenous pyrogen), activates vascular endothelium, and stimulates the production of acute-phase reactants. * **IL-6:** A major mediator of the acute-phase response [1]. It stimulates the liver to produce C-reactive protein (CRP) and promotes the differentiation of B-cells into plasma cells. * **TNF-Alpha:** The "master regulator" of inflammation [1]. It promotes leukocyte adhesion, activates neutrophils, and in high concentrations, can lead to septic shock and cachexia. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-inflammatory Cytokines:** Remember the mnemonic **"TGF-̢ and IL-10"**—these are the two primary "brakes" of the immune system. * **Pyrogenic Cytokines:** IL-1, IL-6, and TNF-̡ are the primary cytokines responsible for inducing fever [1]. * **IL-8:** Specifically functions as a potent **chemotactic factor** for neutrophils ("Clean up on aisle 8") [1]. * **IL-12:** Essential for the differentiation of T-cells into **Th1 cells**, linking innate and adaptive immunity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-99.

Q: Which of the following is NOT a pro-inflammatory cytokine?

PAF. ### Explanation The core of this question lies in the biochemical classification of inflammatory mediators. While all options listed are involved in the inflammatory process, the question specifically asks for a **cytokine** [1]. **Why PAF is the Correct Answer:** **Platelet-Activating Factor (PAF)** is a potent phospholipid-derived mediator (a lipid mediator), not a cytokine [1]. It is synthesized by the action of phospholipase A2 on membrane phospholipids. While PAF is highly pro-inflammatory—causing platelet aggregation, vasodilation, and bronchoconstriction—it belongs to the same category as prostaglandins and leukotrienes, rather than the polypeptide category of cytokines [1]. **Analysis of Incorrect Options:** * **IL-1 (Interleukin-1):** A classic "master" pro-inflammatory cytokine produced mainly by macrophages [1]. It induces fever (endogenous pyrogen) and stimulates the expression of adhesion molecules on endothelial cells [1]. * **IL-8 (CXCL8):** A major pro-inflammatory chemokine [1]. Its primary role is the recruitment and activation of **neutrophils** at the site of inflammation [1]. * **IL-11:** A pleiotropic cytokine of the IL-6 family. While it has some anti-inflammatory properties in specific contexts, it is traditionally classified as a pro-inflammatory cytokine involved in the acute phase response and megakaryocyte maturation. **High-Yield Clinical Pearls for NEET-PG:** * **Major Pro-inflammatory Cytokines:** TNF-α, IL-1, IL-6, and Chemokines (like IL-8) [1]. * **Major Anti-inflammatory Cytokines:** **IL-10** and **TGF-β** (Frequently tested). * **Acute Phase Response:** Primarily driven by IL-6 (the chief stimulator of CRP production in the liver). * **PAF Source:** Derived from the cell membranes of neutrophils, monocytes, and endothelium via the remodeling pathway. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.

Q: What type of ANCA is most commonly associated with Wegener's granulomatosis?

cANCA. **Wegener’s Granulomatosis** (now officially known as **Granulomatosis with Polyangiitis or GPA**) is a small-vessel vasculitis characterized by a triad of necrotizing granulomas of the respiratory tract, necrotizing vasculitis, and focal necrotizing glomerulonephritis [1]. 1. **Why cANCA is correct:** The hallmark laboratory finding in GPA is the presence of **cANCA (cytoplasmic Antineutrophil Cytoplasmic Antibody)** [1]. On immunofluorescence, cANCA shows a diffuse granular cytoplasmic staining pattern. The primary target antigen for cANCA is **Proteinase-3 (PR3)**, a constituent of neutrophil primary granules. It is highly specific (approx. 95%) for GPA, especially when the disease is active. 2. **Why other options are incorrect:** * **pANCA (perinuclear ANCA):** This pattern shows staining around the nucleus and targets the enzyme **Myeloperoxidase (MPO)**. While pANCA is associated with other vasculitides like **Microscopic Polyangiitis (MPA)** and **Churg-Strauss Syndrome (EGPA)**, it is not the primary marker for GPA [1]. * **Both/None:** These are incorrect because the association between cANCA and GPA is distinct and diagnostic in the context of clinical symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Target Antigen:** cANCA = Anti-PR3; pANCA = Anti-MPO. * **Clinical Triad of GPA:** Upper Respiratory Tract (sinusitis/saddle nose deformity), Lower Respiratory Tract (hemoptysis/cavitation), and Kidneys (RPGN). * **Biopsy Gold Standard:** Shows "geographic necrosis" and poorly formed granulomas. * **Monitoring:** ANCA titers often correlate with disease activity; a rise in titers may predict a relapse. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918.

Question 1

A 40-year-old man with a 10-year history of HIV infection presents with newly diagnosed Kaposi sarcoma involving the skin and a 7-kg weight loss in the past 6 months. His HIV-1 RNA viral load is currently 60,000 copies/mL. Which of the following types of cells is most depleted in his lymph nodes?

Accepted Answer

CD4+ lymphocyte

Answer

CD8+ lymphocyte

Answer

CD19+ lymphocyte

Answer

Macrophage

Question 2

A clinical study is performed in which the subjects are children 1 to 4 years old who have had multiple infections with viral, fungal, and parasitic diseases. Compared with a normal control group, these children do not have thymic cells that bear markers of cortical lymphocytes. Which of the following karyotypic abnormalities is most likely to be seen in the children in this study?

Accepted Answer

22q11.2 deletion syndrome

Answer

Trisomy 21

Answer

Philadelphia chromosome (t(9;22))

Answer

Philadelphia chromosome variant (t(15;17))

Question 3

Which of the following can provide the "second signal" to a B-cell bound by a specific antigen?

Accepted Answer

Antigen-specific T-cells

Answer

Epstein-Barr virus

Answer

Endotoxin

Answer

Plasma cells

Question 4

A 40-year-old man presents with yellow skin and sclerae, abdominal tenderness, and dark urine. Physical examination reveals jaundice and mild hepatomegaly. Laboratory studies show elevated serum bilirubin (3.1 mg/dL), decreased serum albumin (2.5 g/dL), and prolonged prothrombin time (17 seconds). Serologic tests reveal antibodies to hepatitis B core antigen (IgG anti-HBcAg). The serum is also positive for HBsAg and HBeAg. What glycoprotein on virally infected hepatocytes provides a target for cell-mediated cytotoxicity in this patient?

Accepted Answer

Class I HLA molecules

Answer

CD4

Answer

CD8

Answer

Class II HLA molecules

Question 5

Which antibody is known to cross the placenta?

Accepted Answer

IgG1

Answer

IgG4

Answer

IgA

Answer

IgD

Question 6

Which of the following cells does HIV primarily affect?

Accepted Answer

Helper T cells

Answer

B-cells

Answer

Suppressor T-cells

Answer

Cytotoxic T-cells

Question 7

Which of the following is NOT a pro-inflammatory cytokine?

Accepted Answer

IL-10

Answer

IL-1

Answer

IL-6

Answer

TNF Alpha

Question 8

Which of the following is NOT a pro-inflammatory cytokine?

Accepted Answer

PAF

Answer

IL-8

Answer

IL-11

Answer

IL-1

Question 9

What type of ANCA is most commonly associated with Wegener's granulomatosis?

Accepted Answer

cANCA

Answer

pANCA

Answer

Both

Answer

None

Question 10

Secondary amyloidosis is a complication of which condition?

Accepted Answer

Rheumatoid arthritis

Answer

Plasmacytosis

Answer

Multiple myeloma

Answer

None of the above

Immunopathology — MCQs

Immunopathology — MCQs

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