Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 281: Which of the following is a pan-T lymphocyte marker?

A. CD2
B. CD3 (Correct Answer)
C. CD19
D. CD25

Explanation: **Explanation:** **CD3** is considered the definitive **pan-T lymphocyte marker** because it is physically associated with the T-cell receptor (TCR) [1]. It is required for the cell-surface expression of the TCR and is involved in the signal transduction pathway following antigen recognition [1]. It is expressed on all mature T-cells (both Helper T-cells and Cytotoxic T-cells) and is the most reliable marker used in immunohistochemistry to identify T-cell lineages [2]. **Analysis of Incorrect Options:** * **CD2:** While CD2 is an early marker found on T-cells and Natural Killer (NK) cells, it is primarily an adhesion molecule (LFA-2) that binds to LFA-3. It is not as specific for the T-cell lineage as CD3. * **CD19:** This is a classic **pan-B lymphocyte marker** [2]. It is expressed on B-cells from the earliest stages of B-cell development until the plasma cell stage [2]. * **CD25:** This is the alpha chain of the **IL-2 receptor**. It is not a pan-marker; rather, it is a marker of **activated T-cells** and is constitutively expressed on **Regulatory T-cells (Tregs)**. **High-Yield Clinical Pearls for NEET-PG:** * **Pan-B markers:** CD19, CD20 (Target of Rituximab), and CD22 [2]. * **NK cell markers:** CD16 (FcγRIII) and CD56. * **Hassall’s Corpuscles:** Found in the thymus; they are characteristic of T-cell maturation sites. * **Flow Cytometry:** The gold standard technique for identifying these clusters of differentiation (CD) markers in leukemias and lymphomas. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 198-199. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 598.

Question 282: Hyperacute graft rejection is caused by which of the following mechanisms?

A. Preformed antibodies (Correct Answer)
B. T-lymphocytes
C. Macrophages
D. B-lymphocytes

Explanation: ### Explanation **Correct Answer: A. Preformed antibodies** **Mechanism of Hyperacute Rejection:** Hyperacute rejection is a **Type II Hypersensitivity reaction**. It occurs within minutes to hours after transplantation. It is mediated by **preformed anti-donor antibodies** (humoral immunity) already present in the recipient's circulation [1]. These antibodies (usually IgG or IgM) bind to antigens on the donor vascular endothelium (such as ABO blood group antigens or HLA Class I molecules). This binding triggers the complement cascade, leading to endothelial injury, fibrin-platelet thrombi formation, and rapid ischemic necrosis of the graft [1]. **Why other options are incorrect:** * **B. T-lymphocytes:** These are primarily responsible for **Acute Cellular Rejection** (Type IV Hypersensitivity) [1]. This typically occurs days to weeks after transplantation, not within minutes. * **C. Macrophages:** While macrophages participate in the inflammatory infiltrate of acute and chronic rejection, they are not the primary initiators of the hyperacute response. * **D. B-lymphocytes:** While B-cells eventually produce antibodies, the hyperacute phase depends on antibodies that are **already present** (preformed) due to prior sensitization (e.g., previous blood transfusions, pregnancies, or failed transplants). **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Grossly, the organ becomes cyanotic, mottled, and flaccid (**"Blue Kidney"**) [1]. Histologically, it shows widespread microvascular thrombosis and neutrophilic infiltration. * **Prevention:** It is prevented by **Cross-matching** (testing recipient serum against donor lymphocytes) and ABO blood group matching. * **Treatment:** There is no effective treatment once it starts; the graft must be removed immediately [1]. * **Timeline Summary:** * **Hyperacute:** Minutes to hours (Preformed Antibodies). * **Acute:** Days to weeks (T-cells/Humoral). * **Chronic:** Months to years (Intimal fibrosis/Arteriosclerosis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242.

Question 283: Cell-mediated lysis of tumor cells is mediated by?

A. HLA Class I (Correct Answer)
B. HLA Class II
C. HLA Class III
D. All of the above

Explanation: **Explanation:** **1. Why HLA Class I is correct:** Cell-mediated immunity against tumor cells primarily involves **CD8+ Cytotoxic T Lymphocytes (CTLs)** [1]. These T cells are specialized to recognize and kill "altered-self" cells, such as those infected by viruses or transformed into tumors. For a CTL to recognize a tumor cell, the tumor-associated antigen must be processed and presented on the cell surface in association with **HLA Class I molecules** (HLA-A, B, or C) [1]. This interaction triggers the release of perforins and granzymes, leading to apoptosis of the tumor cell. **2. Why other options are incorrect:** * **HLA Class II:** These molecules (HLA-DR, DP, DQ) are primarily expressed on **Antigen-Presenting Cells (APCs)** like dendritic cells and macrophages. They present exogenous antigens to **CD4+ Helper T cells** [1]. While CD4+ cells coordinate the immune response, they do not directly mediate the lysis of tumor cells. * **HLA Class III:** These genes encode components of the complement system (C2, C4) and certain cytokines (TNF-α). They are not involved in antigen presentation or direct T-cell recognition. **Clinical Pearls for NEET-PG:** * **Rule of 8:** Remember that MHC I × CD8 = 8 and MHC II × CD4 = 8. * **Tumor Evasion:** One common mechanism by which tumors escape immune surveillance is the **downregulation of HLA Class I expression**, making them "invisible" to CD8+ T cells. * **NK Cells:** If a tumor cell loses HLA Class I expression, it becomes a target for **Natural Killer (NK) cells**, which provide a backup defense mechanism (the "missing self" hypothesis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 318-319.

Question 284: Which of the following statements is not true regarding Churg-Strauss syndrome?

A. Asthma is commonly present.
B. Peripheral eosinophilia is a characteristic finding.
C. It involves vasculitis affecting multiple organ systems.
D. Intravascular granulomas are a typical feature. (Correct Answer)

Explanation: **Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis - EGPA)** is a small-vessel necrotizing vasculitis classically characterized by a triad of asthma, eosinophilia, and extravascular granulomas [1]. ### **Explanation of the Correct Answer** **Option D is the correct answer (the false statement)** because the granulomas in Churg-Strauss syndrome are typically **extravascular** (located in the connective tissue or parenchyma), not intravascular [1]. While the vasculitis affects the vessel walls, the hallmark necrotizing granulomas often form outside the vessels, frequently containing a central core of eosinophilic debris (Charcot-Leyden crystals). ### **Analysis of Incorrect Options** * **Option A:** **Asthma** is the most common initial presentation (prodromal phase) and is present in over 95% of patients [1]. It often precedes the vasculitic phase by years. * **Option B:** **Peripheral eosinophilia** (usually >10% of total WBC count or >1500/µL) is a cardinal diagnostic criterion and reflects the underlying Type I and Type IV hypersensitivity components. * **Option C:** It is a **systemic vasculitis**. While it primarily affects the lungs and skin, it frequently involves the heart (major cause of mortality), gastrointestinal tract, and peripheral nerves (mononeuritis multiplex). ### **NEET-PG High-Yield Pearls** * **ANCA Association:** P-ANCA (anti-MPO) is positive in approximately 40–50% of cases (especially those with renal involvement). * **Key Triad:** Asthma + Peripheral Eosinophilia + Extravascular Granulomas [1]. * **Organ Involvement:** Unlike Wegener’s (GPA), Churg-Strauss rarely involves the upper respiratory tract (sinuses) with the same severity and is strongly linked to **cardiac involvement** (eosinophilic myocarditis). * **Distinction:** Wegener’s = C-ANCA; Churg-Strauss = P-ANCA + Eosinophilia + Asthma. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 322-323.

Question 285: L.E. Cell phenomenon in peripheral blood is seen in:

A. Rheumatic heart disease
B. Infective endocarditis
C. Ischemic heart disease
D. Systemic Lupus Erythematosus (Correct Answer)

Explanation: ### Explanation **1. Why Systemic Lupus Erythematosus (SLE) is Correct:** The **L.E. (Lupus Erythematosus) cell** is a classic laboratory finding historically used to diagnose SLE [1]. It is a neutrophil or macrophage that has ingested the denatured nuclear material of another cell. * **Mechanism:** In SLE, Antinuclear Antibodies (ANA) target the chromatin of damaged cells [1]. This results in the formation of a **hematoxylin body** (a homogenous, purple-blue mass of denatured DNA-histone complex). * **Phagocytosis:** Opsonization by IgG and complement allows a healthy polymorphonuclear leukocyte (neutrophil) to engulf this mass, creating the characteristic L.E. cell. **2. Why the Other Options are Incorrect:** * **A & B (Rheumatic Heart Disease & Infective Endocarditis):** These are inflammatory/infectious conditions. While they involve immune activation, they do not typically involve the specific anti-nucleoprotein antibodies required to produce the L.E. cell phenomenon. * **C (Ischemic Heart Disease):** This is primarily a vascular/mechanical pathology (atherosclerosis/thrombosis) and does not have an autoimmune basis involving ANA. **3. NEET-PG High-Yield Pearls:** * **In Vitro Phenomenon:** The L.E. cell is an *in vitro* phenomenon; it is rarely seen in fresh peripheral blood or skin biopsies. It requires mechanical trauma to cells during blood processing to expose the nuclei. * **Diagnostic Utility:** Though classic, the L.E. cell test is now **obsolete** in clinical practice. It has been replaced by more sensitive and specific tests like **ANA (Indirect Immunofluorescence)** and **Anti-dsDNA** [1]. * **Hematoxylin Bodies:** These are the *in vivo* equivalent of the L.E. phenomenon, often found in heart valves (Libman-Sacks endocarditis) or kidneys of SLE patients. * **Tart Cell:** Do not confuse L.E. cells with "Tart cells" (a monocyte that has ingested a cell nucleus with visible chromatin structure, usually non-specific). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 226.

Question 286: Which of the following statements about acute hemolytic blood transfusion reactions is true?

A. Complement mediated hemolysis is seen. (Correct Answer)
B. Type III hypersensitivity is responsible for most cases.
C. These reactions are rarely life-threatening.
D. Renal blood flow is always maintained.

Explanation: **Explanation:** **Acute Hemolytic Transfusion Reaction (AHTR)** is a medical emergency typically caused by **ABO incompatibility** [2]. 1. **Why Option A is correct:** AHTR is a classic example of **Type II Hypersensitivity**. When incompatible blood is transfused, pre-existing host IgM antibodies (isohemagglutinins) bind to donor red cell antigens. This triggers the **classical complement pathway**, leading to the formation of the Membrane Attack Complex (MAC) [2]. This results in rapid **intravascular hemolysis**, releasing free hemoglobin into the plasma [1]. 2. **Why other options are incorrect:** * **Option B:** AHTR is a **Type II hypersensitivity** (antibody-mediated cytotoxicity), not Type III (immune-complex mediated). * **Option C:** These reactions are **highly life-threatening**. They can rapidly progress to disseminated intravascular coagulation (DIC), shock, and multi-organ failure [2]. * **Option D:** Renal blood flow is **severely compromised**. Free hemoglobin is nephrotoxic and can cause **Acute Tubular Necrosis (ATN)** [1]. Furthermore, systemic hypotension and DIC-induced microthrombi lead to acute renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Clerical/Administrative error (wrong blood to wrong patient) [2]. * **Triad of symptoms:** Fever/Chills, Flank pain (due to renal ischemia), and Hemoglobinuria [1]. * **Lab Findings:** Positive Direct Antiglobulin Test (DAT/Coombs), decreased haptoglobin, and increased indirect bilirubin [1]. * **Management:** Immediate cessation of transfusion and aggressive IV fluid resuscitation to maintain urine output. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 673-674.

Question 287: Hyperacute rejection is due to:

A. Preformed antibodies (Correct Answer)
B. Cytotoxic T-lymphocyte mediated injury
C. Circulating macrophage mediated injury
D. Endothelitis caused by donor antibodies

Explanation: **Explanation:** **Hyperacute rejection** is a Type II hypersensitivity reaction that occurs within minutes to hours after transplantation. 1. **Why Option B is correct:** The reaction is mediated by **preformed antibodies** (IgG) in the recipient's circulation that are specific for antigens on the donor vascular endothelium [1]. These antibodies typically target **ABO blood group antigens** or **HLA molecules** (sensitization from previous transplants, blood transfusions, or pregnancies). Once the graft is vascularized, these antibodies bind to the endothelium, activating the **complement system** and the coagulation cascade [1]. This leads to thrombotic occlusion of the graft vasculature, causing ischemic necrosis (the graft turns "cyanotic" or "mottled" on the operating table) [1]. 2. **Why other options are incorrect:** * **Option B:** Cytotoxic T-lymphocyte (CD8+) mediated injury is the hallmark of **Acute Cellular Rejection**, which typically occurs days to weeks after transplant [1]. * **Option C:** Macrophages are involved in chronic inflammation and delayed-type hypersensitivity but are not the primary mediators of hyperacute rejection. * **Option D:** Endothelitis (inflammation of the endothelium) is a characteristic histological finding in **Acute Antibody-Mediated Rejection**, but it is caused by *recipient* antibodies against donor antigens, not donor antibodies [1]. **High-Yield Pearls for NEET-PG:** * **Histology:** Characterized by widespread microvascular thrombosis, fibrinoid necrosis of vessel walls, and neutrophilic infiltration [1]. * **Prevention:** It is prevented by **Cross-matching** (mixing recipient serum with donor lymphocytes) and ABO typing. * **Treatment:** There is no effective treatment; the graft must be removed immediately [1]. * **Timeline:** Minutes to hours (Immediate). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242.

Question 288: Graft vs Host reaction can be reduced by which of the following methods?

A. Irradiation (Correct Answer)
B. Leukoreduction/Leukofiltration
C. Immunosuppression
D. Buffy coat removal

Explanation: **Explanation:** **Graft-versus-Host Disease (GVHD)**, specifically Transfusion-Associated GVHD (TA-GVHD), occurs when viable donor T-lymphocytes engraft and mount an immune attack against the recipient’s tissues [1]. This is particularly fatal in immunocompromised patients or when there is a partial HLA match between donor and recipient. **Why Irradiation is the Correct Answer:** Gamma irradiation (usually 25-30 Gy) is the **gold standard** for preventing TA-GVHD. It works by inducing DNA cross-linking in donor lymphocytes, which inhibits their ability to proliferate (mitotic arrest) without damaging the functional integrity of red cells, platelets, or granulocytes. Since the pathogenesis of GVHD depends on the proliferation of donor T-cells, stopping their division effectively prevents the reaction. **Analysis of Incorrect Options:** * **Leukoreduction/Leukofiltration:** While this process removes the majority of WBCs to prevent febrile non-hemolytic transfusion reactions (FNHTR) and CMV transmission, it does **not** remove enough lymphocytes to prevent GVHD. A residual amount of viable T-cells can still trigger a reaction. * **Immunosuppression:** While used to *treat* GVHD once it occurs, it is not the primary method for *reducing the risk* in blood products prior to transfusion [1]. * **Buffy coat removal:** This reduces the number of leukocytes but is far less efficient than leukofiltration and insufficient to prevent GVHD. **High-Yield Clinical Pearls for NEET-PG:** * **Indications for Irradiation:** Bone marrow transplant recipients, Hodgkin lymphoma, neonates (exchange transfusion), and directed donations from first-degree relatives. * **Shelf-life:** Irradiated RBCs have a reduced shelf-life (maximum 28 days) due to increased potassium leakage from the cells. * **TA-GVHD vs. Transplant GVHD:** TA-GVHD is nearly always fatal (90%+ mortality) because it involves an attack on the recipient's bone marrow, leading to pancytopenia. **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 289: What is the first line of defense against tumors and viruses?

A. NK cell (Correct Answer)
B. T cell
C. Histiocyte
D. Macrophage

Explanation: **NK (Natural Killer) cells** are the correct answer because they serve as the body's **first line of defense** against both virally infected cells and tumor cells [1], [2]. Unlike T cells, NK cells are part of the **innate immune system** [3]. They do not require prior sensitization or MHC-restricted antigen presentation to function. They operate via the "missing self" hypothesis: they identify and kill cells that have downregulated MHC Class I molecules—a common strategy used by viruses and tumors to evade detection by cytotoxic T lymphocytes (CTLs) [1]. **Analysis of Incorrect Options:** * **T cells (Option B):** These are part of the adaptive immune system. While CD8+ T cells are highly effective at killing tumors and viruses, they require time for activation, clonal expansion, and MHC-restricted antigen presentation. Thus, they represent a secondary, specific response rather than the "first line." * **Histiocytes (Option C):** This is a general term for tissue-resident macrophages or dendritic cells. While they act as antigen-presenting cells (APCs), they are not the primary effectors for direct tumor lysis. * **Macrophages (Option D):** While they participate in the innate response and can phagocytose debris or secrete TNF-̑, they are primarily scavengers and regulators. They are not as specialized or rapid as NK cells in the direct lysis of tumor and viral targets. **High-Yield Clinical Pearls for NEET-PG:** * **Markers:** NK cells are identified by **CD16** (Fc̑RIII, which mediates Antibody-Dependent Cellular Cytotoxicity - ADCC) and **CD56** (NCAM). * **Mechanism:** They use **perforins** and **granzymes** to induce apoptosis. * **Cytokine Activation:** Their activity is significantly enhanced by **IL-2, IL-12, and IFN-̑/̒** [1]. * **Clinical Correlation:** Deficiency in NK cell function is associated with an increased incidence of lymphomas and recurrent viral infections (especially Herpesviridae). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201, 207-208, 194-196. [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. 164-165. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 194-196.

Question 290: Which of the following is caused by C1 inhibitor deficiency?

A. Hereditary angioneurotic edema (Correct Answer)
B. Systemic lupus erythematosus
C. Severe recurrent pyogenic infection
D. Collagen vascular disease

Explanation: **Explanation:** **Hereditary Angioneurotic Edema (HAE)** is the correct answer because it is caused by an inherited deficiency (Type I) or dysfunction (Type II) of the **C1 inhibitor (C1-INH)**. C1-INH is a serine protease inhibitor that normally regulates the classical complement pathway by inhibiting C1r and C1s. Crucially, it also inhibits **kallikrein** and **Factor XII** in the kinin system. Its deficiency leads to the uncontrolled activation of the kallikrein-kinin cascade, resulting in excessive production of **bradykinin**. Bradykinin increases vascular permeability, leading to episodes of non-pitting edema in the skin, larynx, and gastrointestinal tract [1]. **Analysis of Incorrect Options:** * **Systemic Lupus Erythematosus (SLE):** While SLE is associated with complement deficiencies, it is specifically linked to early components of the classical pathway (**C1q, C4, or C2**) [2]. These deficiencies impair the clearance of immune complexes. * **Severe recurrent pyogenic infection:** This is typically seen in **C3 deficiency**, as C3 is central to opsonization and the convergence of all complement pathways [3]. Deficiencies in MAC components (C5-C9) lead to *Neisseria* infections. * **Collagen vascular disease:** This is a broad category (including SLE and Rheumatoid Arthritis). While complement consumption occurs during active disease, C1-INH deficiency is not the primary cause. **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Marker:** The screening test of choice for HAE is a **low C4 level**, even during asymptomatic periods. * **Clinical Contraindication:** Patients with C1-INH deficiency should avoid **ACE inhibitors**, as they prevent bradykinin breakdown and can precipitate life-threatening angioedema [1]. * **Treatment:** Acute attacks are managed with C1-INH concentrate or **Icatibant** (bradykinin B2 receptor antagonist). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-926. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 534-535.

Practice by Chapter

Cells and Tissues of the Immune System

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Innate Immunity

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Adaptive Immunity

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Hypersensitivity Reactions

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Autoimmune Diseases

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Immunodeficiency Disorders

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Transplantation Immunopathology

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Immune Response to Infections

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Immunologic Laboratory Techniques

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Tumor Immunology

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