Immunopathology Practice Questions

Q: Type V hypersensitivity is a type of:

Type II hypersensitivity. ### Explanation **Correct Answer: B. Type II hypersensitivity** **Mechanism:** Type V hypersensitivity is considered a **subtype of Type II hypersensitivity** (Antibody-mediated cytotoxicity). While standard Type II involves antibodies (IgG or IgM) causing cell destruction or inflammation, Type V is specifically characterized by **stimulatory antibodies**. These antibodies bind to cell surface receptors and mimic the natural ligand, leading to continuous activation of the cell rather than its destruction. **Why Type II is correct:** The Gell and Coombs classification originally described four types. Type V was later added to describe "Stimulatory Hypersensitivity." Since it involves antibodies directed against specific cell-surface antigens (receptors), it is functionally a modification of the Type II mechanism. **Why other options are incorrect:** * **Type I:** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Atopy). * **Type III:** Mediated by the deposition of soluble Antigen-Antibody (Immune) complexes in tissues (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type IV:** A delayed-type hypersensitivity mediated by T-cells, not antibodies (e.g., Mantoux test, Contact dermatitis). **Clinical Pearls for NEET-PG:** * **Classic Example:** **Graves’ Disease**, where Long-Acting Thyroid Stimulators (LATS/TSH-receptor antibodies) stimulate the thyroid gland to produce excess T3/T4. * **Another Example:** **Myasthenia Gravis** (though usually inhibitory, it involves antibodies against ACh receptors). * **Key Distinction:** Unlike other Type II reactions, Type V does **not** involve complement activation or cell lysis.

Q: Hyperacute graft rejection is a manifestation of which type of hypersensitivity?

Type II hypersensitivity. **Explanation:** **Hyperacute rejection** occurs within minutes to hours after transplantation. It is a classic example of **Type II (Antibody-mediated) Hypersensitivity**. * **Mechanism:** It is mediated by **pre-formed cytotoxic antibodies** (IgG or IgM) in the recipient’s serum that react against antigens on the donor vascular endothelium. These antibodies are usually directed against ABO blood group antigens or HLA Class I antigens. * **Pathophysiology:** The binding of these antibodies triggers the **complement cascade**, leading to endothelial damage, platelet aggregation, and diffuse intravascular coagulation. This results in rapid thrombosis and ischemic necrosis of the graft (classically described as a "shrunken, purple kidney" on the operating table). **Why other options are incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). It is not involved in graft rejection. * **Type III (Immune-complex):** Involves deposition of antigen-antibody complexes in tissues (e.g., SLE, Serum Sickness). While some chronic rejection components involve complexes, hyperacute rejection is a direct cytotoxic attack. * **Type IV (Delayed-type):** Mediated by T-cells. This is the mechanism behind **Acute Rejection** (days to weeks) and **Chronic Rejection** (months to years), but not hyperacute. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** Hyperacute rejection is prevented by **cross-matching** (testing recipient serum against donor lymphocytes). * **Histology:** Characterized by neutrophilic infiltration of arterioles and fibrinoid necrosis. * **Treatment:** There is no effective treatment once it begins; the graft must be removed immediately. * **Common Scenarios:** Usually seen in patients with prior blood transfusions, multiple pregnancies, or previous transplants (sensitization).

Q: All of the following are immune complex diseases except?

Graft rejection. **Explanation:** The question tests the classification of hypersensitivity reactions. The correct answer is **Graft rejection** because it is primarily a **Type IV (Cell-mediated) hypersensitivity reaction**, whereas the other options are examples of **Type III (Immune complex-mediated) hypersensitivity**. **1. Why Graft Rejection is the Correct Answer:** Acute graft rejection is mediated by T-lymphocytes (CD8+ cytotoxic T cells and CD4+ helper T cells) reacting against donor MHC antigens. While hyperacute rejection involves pre-formed antibodies (Type II), the classic process of rejection is the hallmark of Type IV hypersensitivity, not the deposition of circulating immune complexes. **2. Analysis of Incorrect Options (Type III Hypersensitivity):** * **Serum Sickness:** A systemic Type III reaction occurring when foreign serum proteins are injected. Antigen-antibody complexes form in the blood and deposit in tissues (joints, kidneys), causing fever, rash, and arthritis. * **Farmer’s Lung:** A form of Hypersensitivity Pneumonitis. It occurs when inhaled fungal spores (e.g., *Saccharopolyspora rectivirgula*) react with specific IgG antibodies, forming local immune complexes in the alveoli. * **Systemic Lupus Erythematosus (SLE):** The prototype of systemic Type III hypersensitivity. Auto-antibodies bind to self-antigens (like DNA), forming complexes that deposit in small vessels, leading to glomerulonephritis and vasculitis. **High-Yield Clinical Pearls for NEET-PG:** * **Type III mnemonic:** "Immune Complex" (Ag-Ab complexes + Complement activation). * **Arthus Reaction:** A localized Type III reaction (e.g., swelling after a booster vaccine). * **Key Triad of Serum Sickness:** Fever, Urticaria, and Arthralgia. * **Graft vs. Host Disease (GVHD):** Occurs when donor T-cells attack the recipient's tissues; also a Type IV reaction.

Q: Which cytokine enhances NK cell activity?

Interleukin-2 (IL-2). **Explanation:** The correct answer is **Interleukin-2 (IL-2)**. Natural Killer (NK) cells are innate immune lymphocytes that provide the first line of defense against virally infected cells and tumor cells. Their activation and proliferation are heavily dependent on specific cytokines. **IL-2**, primarily secreted by CD4+ T-helper (Th1) cells, acts as a potent growth factor for both T-cells and NK cells [1]. It enhances the cytotoxic capacity of NK cells and induces their differentiation into **Lymphokine-Activated Killer (LAK) cells**, which have superior anti-tumor activity. **Analysis of Options:** * **IL-1 (Option A):** A pro-inflammatory cytokine produced by macrophages. Its primary roles include inducing fever (pyrogen), activating vascular endothelium, and stimulating the synthesis of acute-phase reactants. * **TNF (Option B):** Primarily involved in systemic inflammation, induction of apoptosis, and recruitment of leukocytes. While it works synergistically with other cytokines, it is not the primary enhancer of NK cell activity. * **TGF-β (Option D):** Generally an **immunosuppressive** cytokine. It inhibits lymphocyte proliferation and suppresses NK cell activity, acting as a "brake" on the immune response. **NEET-PG High-Yield Pearls:** * **IL-2, IL-12, IL-15, and Type I Interferons (IFN-α/β)** are the primary stimulators of NK cells [1]. * **IL-12** is the most potent inducer of **IFN-γ** production by NK cells [1]. * NK cells do not require prior sensitization and lack MHC restriction (they follow the "missing self" hypothesis). * **Clinical Correlation:** Recombinant IL-2 (Aldesleukin) has been used in immunotherapy for renal cell carcinoma and melanoma due to its ability to boost NK and T-cell responses. **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.

Q: A 54-year-old woman with rheumatoid arthritis presents with a 2-year history of dry eyes and dry mouth. Physical examination confirms xerostomia and xerophthalmia and reveals enlarged lacrimal glands bilaterally. Histologic examination of the lacrimal glands would likely show an infiltrate of which of the following inflammatory cell types?

Lymphocytes. The clinical presentation of dry eyes (**xerophthalmia**) and dry mouth (**xerostomia**) in a patient with an existing autoimmune condition like Rheumatoid Arthritis (RA) is diagnostic of **Secondary Sjögren’s Syndrome** [1]. 1. **Why Lymphocytes are correct:** Sjögren’s syndrome is a chronic autoimmune epithelitis characterized by the progressive destruction of exocrine glands (lacrimal and salivary). The hallmark histopathological feature is a **periductal lymphocytic infiltrate**, primarily consisting of **CD4+ T-helper cells** and some B cells. These lymphocytes form "foci" that replace the normal glandular parenchyma, leading to secretory dysfunction and gland enlargement. 2. **Why other options are incorrect:** * **Fibroblasts:** While chronic inflammation can eventually lead to fibrosis in late-stage disease, the primary diagnostic infiltrate is inflammatory (lymphocytic), not fibroblastic. * **Macrophages:** These are seen in granulomatous diseases (like Sarcoidosis) or chronic non-specific inflammation, but they are not the predominant cell type in Sjögren’s. * **Mast cells:** These are associated with Type I hypersensitivity (allergic) reactions, not the Type IV delayed-type hypersensitivity seen in Sjögren’s. **High-Yield Clinical Pearls for NEET-PG:** * **Schirmer’s Test:** Used to quantify decreased tear production (<5 mm in 5 mins is positive). * **Serology:** Anti-Ro (SS-A) and Anti-La (SS-B) antibodies are highly specific. * **Biopsy Gold Standard:** Lip biopsy (minor salivary gland biopsy) showing lymphocytic foci (Focus score ≥1). * **Malignancy Risk:** Patients with Sjögren’s have a **40-fold increased risk of B-cell Non-Hodgkin Lymphoma** (typically MALT lymphoma). * **Extraglandular manifestation:** Most common is arthralgia/arthritis; others include Raynaud’s and interstitial nephritis.

Question 1

Type V hypersensitivity is a type of:

Accepted Answer

Type II hypersensitivity

Answer

Type I hypersensitivity

Answer

Type III hypersensitivity

Answer

Type IV hypersensitivity

Question 2

Which of the following is an organ-specific autoimmune disease?

Accepted Answer

Goodpasture's syndrome

Answer

Systemic Lupus Erythematosus (SLE)

Answer

Rheumatoid Arthritis (RA)

Answer

Polyarteritis Nodosa (PAN)

Question 3

Hyperacute graft rejection is a manifestation of which type of hypersensitivity?

Accepted Answer

Type II hypersensitivity

Answer

Type I hypersensitivity

Answer

Type III hypersensitivity

Answer

Type IV hypersensitivity

Question 4

All of the following are immune complex diseases except?

Accepted Answer

Graft rejection

Answer

Serum sickness

Answer

Farmer's lung

Answer

Systemic lupus erythematosus

Question 5

Which cytokine enhances NK cell activity?

Accepted Answer

Interleukin-2 (IL-2)

Answer

Interleukin-1 (IL-1)

Answer

Tumor Necrosis Factor (TNF)

Answer

Transforming Growth Factor-beta (TGF-b)

Question 6

Rejection that may appear within minutes or hours of transplantation is termed as:

Accepted Answer

Hyperacute Rejection

Answer

Acute cellular (T cell-mediated) rejection

Answer

Acute antibody-mediated rejection

Answer

Chronic Rejection

Question 7

A 54-year-old woman with rheumatoid arthritis presents with a 2-year history of dry eyes and dry mouth. Physical examination confirms xerostomia and xerophthalmia and reveals enlarged lacrimal glands bilaterally. Histologic examination of the lacrimal glands would likely show an infiltrate of which of the following inflammatory cell types?

Accepted Answer

Lymphocytes

Answer

Fibroblasts

Answer

Macrophages

Answer

Mast cells

Question 8

Hyperacute rejection of renal transplant is which type of hypersensitivity reaction?

Accepted Answer

Type II hypersensitivity reaction

Answer

Type I hypersensitivity reaction

Answer

Type III hypersensitivity reaction

Answer

Type IV hypersensitivity reaction

Question 9

Which of the following conditions is primarily a T-cell mediated disease?

Accepted Answer

Sarcoidosis

Answer

Asthma

Answer

Myasthenia gravis

Answer

Systemic Lupus Erythematosus (SLE)

Question 10

Which of the following is NOT true about graft-versus-host reaction?

Accepted Answer

None of the above statements are untrue (i.e., all are true about GvHD)

Answer

The question asks for an untrue statement regarding graft-versus-host reaction.

Answer

Bile duct damage

Answer

Intrahepatic cholestasis

Immunopathology — MCQs

Immunopathology — MCQs

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