Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 231: What is amyloidosis?

A. RNA misfolding
B. DNA repair defect
C. Mitochondrial defect
D. Protein misfolding (Correct Answer)

Explanation: **Explanation:** **Amyloidosis** is a clinical disorder characterized by the extracellular deposition of abnormal, insoluble fibrils known as **amyloid** [1]. The fundamental pathogenesis lies in **protein misfolding**. Normally, proteins are folded into specific three-dimensional shapes; however, in amyloidosis, proteins undergo structural changes (often due to mutations or excessive production) that cause them to adopt a **cross-̠-pleated sheet** configuration [3]. These misfolded proteins aggregate, become resistant to proteolysis, and deposit in tissues, leading to organ dysfunction [2]. **Analysis of Options:** * **A (RNA misfolding):** RNA is involved in protein synthesis (translation), but the pathological hallmark of amyloidosis is the final protein product's structural failure, not the RNA itself. * **B (DNA repair defect):** These defects (e.g., Xeroderma Pigmentosum) lead to genomic instability and cancer, not the deposition of fibrillar proteins. * **C (Mitochondrial defect):** These typically result in metabolic or energy-failure diseases (e.g., MELAS) rather than extracellular protein aggregation. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red** [3]. * **Morphology:** On H&E stain, it appears as an extracellular, amorphous, eosinophilic (pink) hyaline material [2]. * **Common Types:** * **AL (Amyloid Light Chain):** Associated with Multiple Myeloma (Plasma cell dyscrasias) [4]. * **AA (Amyloid Associated):** Associated with chronic inflammation (e.g., RA, Tuberculosis). * **Transthyretin (TTR):** Seen in Senile Systemic Amyloidosis and Familial Amyloid Polyneuropathies. * **Diagnosis:** Abdominal fat pad biopsy or rectal biopsy are common screening procedures. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-266. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 533-534. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267.

Question 232: ABO incompatibility is an example of which hypersensitivity reaction?

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

Explanation: **Explanation:** **Why Type-II Hypersensitivity is Correct:** Type-II hypersensitivity is **antibody-mediated cytotoxicity**. It occurs when IgG or IgM antibodies bind to specific antigens located on the **surface of cells** or extracellular matrix [1]. In ABO incompatibility (e.g., a mismatched blood transfusion), pre-existing IgM antibodies (isohemagglutinins) in the recipient's plasma bind to A or B antigens on the donor's red blood cells (RBCs). This triggers the **classical complement pathway**, leading to the formation of the Membrane Attack Complex (MAC) and subsequent **intravascular hemolysis**. **Analysis of Incorrect Options:** * **Type-I (Immediate):** Mediated by **IgE** antibodies and mast cell degranulation (e.g., Anaphylaxis, Asthma, Urticaria) [2]. ABO reactions do not involve IgE. * **Type-III (Immune-complex):** Caused by deposition of **soluble** antigen-antibody complexes in tissues (e.g., SLE, Post-streptococcal glomerulonephritis) [3]. In ABO reactions, the antigen is fixed on the cell surface, not soluble. * **Type-IV (Delayed):** Mediated by **T-cells** (CD4+ or CD8+), not antibodies (e.g., Mantoux test, Contact dermatitis). ABO reactions are rapid and antibody-driven. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Type-II:** Remember **"Cyto-toxic"** (Cell-targeted). * **Other Examples of Type-II:** Rh incompatibility (Erythroblastosis fetalis), Goodpasture syndrome, Myasthenia gravis, Graves' disease, and Autoimmune Hemolytic Anemia (AIHA). * **Key Mechanism:** Complement-mediated lysis, Opsonization (phagocytosis), or Antibody-dependent cellular cytotoxicity (ADCC) [1]. * **Direct Coombs Test:** Used to detect antibodies or complement proteins already bound to the surface of RBCs in Type-II reactions. **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] 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. 171-172. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215.

Question 233: Which of the following is an immune privilege site?

A. Seminiferous tubule (Correct Answer)
B. Optic nerve
C. Area postrema
D. Spinal canal

Explanation: **Explanation:** **Immune privilege** is a physiological adaptation that allows certain tissues to tolerate the introduction of antigens without eliciting an inflammatory immune response. This mechanism protects vital organs from damage caused by the body's own immune system. **Why Option A is Correct:** The **seminiferous tubules** (testis) are a classic example of an immune privilege site [1]. This is maintained by the **Blood-Testis Barrier (BTB)**, formed by tight junctions between **Sertoli cells**. This barrier sequesters developing germ cells (which express neo-antigens during meiosis) from the systemic circulation. Additionally, the local microenvironment produces immunosuppressive cytokines (like TGF-β) and expresses Fas-ligand to induce apoptosis in infiltrating T-cells. **Analysis of Incorrect Options:** * **B. Optic nerve:** While the **anterior chamber of the eye** and the **cornea** are immune-privileged [1], the optic nerve itself is part of the CNS but is not considered a primary "privileged site" in the same context as the intraocular compartments. * **C. Area postrema:** This is one of the **Circumventricular Organs (CVOs)**. Unlike most of the brain, it lacks a blood-brain barrier (BBB) to allow for the sensing of toxins in the blood, making it more exposed to the immune system, not less. * **D. Spinal canal:** While the CNS has some degree of privilege due to the BBB, the "canal" is a space containing CSF. The privilege is attributed to the **Brain Parenchyma**, not the canal itself. **High-Yield Clinical Pearls for NEET-PG:** * **Key Immune Privilege Sites:** Eye (Anterior chamber), Testis, Brain, Placenta/Fetus, and Hair Follicles [1]. * **Clinical Correlation:** Trauma to one eye can release sequestered antigens, leading to an autoimmune attack on the uninjured eye, a condition known as **Sympathetic Ophthalmia**. * **Mechanism:** Privilege is maintained by physical barriers, low expression of MHC Class I molecules, and increased expression of inhibitory molecules (FasL, PD-L1). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 385-386.

Question 234: Hyperacute rejection is due to:

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

Explanation: ### Explanation **Correct Option: A. Preformed antibodies** **Hyperacute rejection** is a Type II hypersensitivity reaction that occurs within minutes to hours after transplantation. It is mediated by **preformed circulating antibodies** in the recipient's blood that are specific for antigens on the graft endothelium. These antibodies (usually anti-ABO or anti-HLA) bind immediately to the donor vascular endothelium, triggering the complement cascade, leading to thrombosis, fibrinoid necrosis, and ischemic necrosis of the graft [1]. **Analysis of Incorrect Options:** * **B. Cytotoxic T-lymphocyte (CTL) mediated injury:** This is the hallmark of **Acute Cellular Rejection**. It typically occurs days to weeks after transplantation and involves CD8+ T-cells attacking the graft parenchyma [1]. * **C. Circulating macrophage mediated injury:** While macrophages play a role in chronic inflammation and delayed-type hypersensitivity, they are not the primary mediators of hyperacute rejection. * **D. Endothelialitis caused by donor antibodies:** Endothelialitis (inflammation of the vessel wall) is a feature of **Acute Antibody-Mediated Rejection** [1]. In hyperacute rejection, the antibodies are from the **recipient**, not the donor. **High-Yield Clinical Pearls for NEET-PG:** * **Gross Appearance:** The graft rapidly becomes cyanotic, mottled, and flaccid (often described as a "blue kidney") [1]. * **Prevention:** This type of rejection is now rare due to mandatory **cross-matching** (testing recipient serum against donor lymphocytes) and ABO blood grouping before surgery. * **Key Histopathology:** Widespread microvascular thrombosis and **neutrophilic infiltration** within the peritubular capillaries [1]. * **Timeline Summary:** * **Hyperacute:** Minutes/Hours (Preformed antibodies). * **Acute:** Days/Weeks (T-cells or Antibodies). * **Chronic:** Months/Years (Vascular intimal thickening and fibrosis). **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 235: A 30-year-old man presents with fever, chills, and neck stiffness. Cerebrospinal fluid analysis reveals gram-negative diplococci. The patient has a history of sepsis with meningococcemia. Which immunologic deficiency is most likely responsible?

A. Complement deficiency C5-C9 (Correct Answer)
B. Post-splenectomy status
C. Drug-induced agranulocytosis
D. Interleukin-12 receptor deficit

Explanation: The clinical presentation of fever, neck stiffness, and Gram-negative diplococci (*Neisseria meningitidis*) in a patient with a history of recurrent sepsis strongly suggests a deficiency in the **Membrane Attack Complex (MAC)**. [1] **1. Why Option A is Correct:** The complement components **C5, C6, C7, C8, and C9** assemble to form the Membrane Attack Complex (MAC). The MAC is essential for the lysis of thin-walled bacteria, specifically the *Neisseria* species (*N. meningitidis* and *N. gonorrhoeae*). Patients with deficiencies in these terminal components are unable to eliminate these pathogens effectively, leading to a significantly increased risk (up to 10,000-fold) of recurrent disseminated neisserial infections. **2. Why Other Options are Incorrect:** * **B. Post-splenectomy status:** While the spleen is vital for clearing encapsulated organisms (e.g., *S. pneumoniae*, *H. influenzae*), the specific recurrence of *Neisseria* in the absence of other infections more classically points to complement defects. * **C. Drug-induced agranulocytosis:** This leads to a generalized susceptibility to various bacterial and fungal infections due to a lack of neutrophils, not specifically *Neisseria*. * **D. Interleukin-12 receptor deficit:** This impairs Th1 responses and IFN-γ production, leading to increased susceptibility to **mycobacterial** (atypical and BCG) and salmonella infections. **High-Yield Clinical Pearls for NEET-PG:** * **C1, C2, C4 deficiency:** Associated with Immune Complex diseases like **Systemic Lupus Erythematosus (SLE)**. * **C3 deficiency:** Most severe; leads to recurrent infections with **all types of pyogenic bacteria** and Type III hypersensitivity. * **C1 Esterase Inhibitor deficiency:** Causes **Hereditary Angioedema** (characterized by low C4 levels). * **DAF (CD55) deficiency:** Leads to **Paroxysmal Nocturnal Hemoglobinuria (PNH)**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1274-1275.

Question 236: C-ANCA positivity indicates antibody formation against which antigen?

A. Proteinase 3 (Correct Answer)
B. Myeloperoxidase
C. Cytoplasmic antinuclear antibody
D. Anti centromere antibody

Explanation: **Explanation:** The **Antineutrophil Cytoplasmic Antibody (ANCA)** test is a crucial diagnostic marker for small-vessel vasculitides. Based on immunofluorescence patterns, ANCAs are divided into two main types [2]: 1. **C-ANCA (Cytoplasmic pattern):** This shows a diffuse granular staining of the neutrophil cytoplasm. The primary target antigen is **Proteinase 3 (PR3)**, a neutral serine protease found in the azurophilic granules of neutrophils. 2. **P-ANCA (Perinuclear pattern):** This shows staining around the nucleus. The primary target antigen is **Myeloperoxidase (MPO)**. **Analysis of Options:** * **Option A (Correct):** C-ANCA is highly specific (approx. 90%) for **Granulomatosis with Polyangiitis (GPA)**, formerly known as Wegener’s Granulomatosis. The antibodies are directed against **Proteinase 3**. * **Option B (Incorrect):** Myeloperoxidase (MPO) is the target antigen for **P-ANCA**, which is associated with Microscopic Polyangiitis (MPA), Churg-Strauss Syndrome (EGPA), and Primary Sclerosing Cholangitis. * **Option C (Incorrect):** "Cytoplasmic antinuclear antibody" is a misnomer. ANCA stands for Antineutrophil Cytoplasmic Antibody [3]; it is distinct from ANA (Antinuclear Antibody). * **Option D (Incorrect):** Anti-centromere antibodies are characteristic of **CREST syndrome** (Limited Systemic Sclerosis), not vasculitis. **High-Yield Clinical Pearls for NEET-PG:** * **C-ANCA/PR3:** Most specific for **Granulomatosis with Polyangiitis (GPA)** [1]. Remember the "C" for "C-shape" of the respiratory tract (Upper/Lower) and "C" for C-ANCA. * **P-ANCA/MPO:** Associated with **Microscopic Polyangiitis** and **Churg-Strauss Syndrome**. * **Monitoring:** C-ANCA titers often correlate with disease activity in GPA; a rising titer may predict a relapse. * **Drug-induced Lupus:** Often associated with anti-histone antibodies, whereas P-ANCA can sometimes be seen in drug-induced vasculitis (e.g., Hydralazine, Propylthiouracil). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 513-514. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279.

Question 237: Necrotizing arteritis with fibrinoid necrosis is mediated by which of the following?

A. Immediate hypersensitivity
B. Cell-mediated immunity
C. Antigen-antibody complex (Correct Answer)
D. Cytotoxic cell-mediated

Explanation: **Explanation:** **Necrotizing arteritis with fibrinoid necrosis** is the hallmark pathological feature of **Type III Hypersensitivity (Immune Complex-Mediated).** [1] **Why Option C is Correct:** In Type III hypersensitivity, circulating **antigen-antibody complexes** deposit in the walls of blood vessels. [1] These complexes activate the **complement system** (classical pathway), leading to the release of C3a and C5a (anaphylatoxins). [3] This recruits neutrophils, which release lysosomal enzymes and reactive oxygen species, causing damage to the vessel wall. [4] The leakage of plasma proteins (including fibrin) into the damaged vessel wall, combined with necrotic debris, creates a smudgy, eosinophilic appearance under the microscope known as **fibrinoid necrosis**. [5] **Why Other Options are Incorrect:** * **Option A (Immediate Hypersensitivity):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). It does not typically cause necrotizing vasculitis. * **Option B & D (Cell-mediated/Cytotoxic):** These represent **Type IV Hypersensitivity**, mediated by T-cells (CD4+ or CD8+). While they cause granulomatous inflammation (e.g., TB, Sarcoidosis), they are not the primary mechanism for acute necrotizing arteritis with fibrinoid necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Examples:** Polyarteritis Nodosa (PAN), Systemic Lupus Erythematosus (SLE), and Arthus reaction. [2] * **Microscopic Appearance:** Fibrinoid necrosis appears as a **bright pink (eosinophilic)**, circumferential ring within the vessel wall. * **Key Mediator:** Complement activation (C5a) and subsequent **neutrophilic** infiltration are crucial for the development of the lesion. [4] * **Exception:** In ANCA-associated vasculitis (like GPA), fibrinoid necrosis occurs but is often "pauci-immune" (minimal antibody deposition). [4] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216. [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. 172-173. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 514-515.

Question 238: All of the following statements regarding Antineutrophil Cytoplasmic Antibodies (ANCA) are true, EXCEPT:

A. Proteinase-3, found in neutrophil azurophilic granules, is the primary antigen for cANCA.
B. Myeloperoxidase is the main target antigen for pANCA.
C. A pANCA staining pattern is linked to nonvasculitic conditions, including rheumatic and other autoimmune diseases.
D. There are three principal classifications of ANCA. (Correct Answer)

Explanation: **Explanation:** The correct answer is **D** because there are only **two** principal classifications of ANCA based on immunofluorescence patterns: **cANCA** (cytoplasmic) and **pANCA** (perinuclear). While a third pattern, xANCA (atypical), is sometimes described in inflammatory bowel disease, it is not considered a "principal" classification in the context of systemic vasculitis. **Analysis of Options:** * **Option A (Incorrect):** This is a true statement. **Proteinase-3 (PR3)** is the major antigen for cANCA. It is located in the azurophilic granules of neutrophils. cANCA is highly specific (approx. 90%) for **Granulomatosis with Polyangiitis (Wegener's)**. * **Option B (Incorrect):** This is a true statement. **Myeloperoxidase (MPO)** is the primary target for pANCA [1]. It is associated with Microscopic Polyangiitis (MPA), Churg-Strauss Syndrome (EGPA), and Pauci-immune Crescentic Glomerulonephritis [1]. * **Option C (Incorrect):** This is a true statement. Unlike cANCA, which is highly specific for vasculitis, **pANCA** can be found in non-vasculitic conditions such as Primary Sclerosing Cholangitis (PSC), Ulcerative Colitis, and Rheumatoid Arthritis. **High-Yield Clinical Pearls for NEET-PG:** * **cANCA/PR3-ANCA:** Associated with Granulomatosis with Polyangiitis (GPA). * **pANCA/MPO-ANCA:** Associated with Microscopic Polyangiitis (MPA) and Eosinophilic Granulomatosis with Polyangiitis (EGPA) [1]. * **Diagnostic Gold Standard:** The current recommendation is to use **ELISA** to confirm the specific antigen (PR3 or MPO) after an initial screening with **Indirect Immunofluorescence (IIF)**. * **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 239: Which of the following tests should be done to optimize graft uptake in bone marrow transplant?

A. Blood grouping
B. HLA matching (Correct Answer)
C. Culture for infection
D. All of the above

Explanation: **Explanation:** The success of a **Bone Marrow Transplant (BMT)** or Hematopoietic Stem Cell Transplant (HSCT) depends primarily on the degree of **HLA (Human Leukocyte Antigen) matching** between the donor and the recipient [1]. **Why HLA Matching is the Correct Answer:** HLA molecules (MHC Class I and II) are the primary determinants of "self" vs. "non-self." [3] In BMT, unlike solid organ transplants, the donor's immune system is being transferred into the recipient. If HLA antigens are not closely matched, two major complications occur: 1. **Graft Rejection:** The recipient’s residual immune system attacks the donor cells [1]. 2. **Graft-versus-Host Disease (GVHD):** The donor’s T-cells recognize the recipient’s tissues as foreign and attack them [2]. High-resolution HLA matching (specifically at HLA-A, B, C, and DRB1 loci) is the gold standard to optimize uptake and minimize GVHD. **Analysis of Incorrect Options:** * **Blood Grouping (ABO):** While essential for blood transfusions, ABO incompatibility is **not** a contraindication for BMT. Since the recipient’s hematopoiesis will eventually be replaced by the donor's, BMT can be performed across ABO barriers with appropriate processing. * **Culture for Infection:** While screening for infections (like HIV, Hepatitis, or CMV) is a standard pre-transplant safety protocol, it does not "optimize graft uptake" or biological compatibility [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Best Donor:** An HLA-identical sibling is the preferred donor (25% chance of a match among siblings). * **GVHD Target Organs:** Skin (rash), Liver (jaundice), and GI tract (diarrhea) [2]. * **Graft-versus-Leukemia (GVL) effect:** A beneficial side effect where donor T-cells eliminate residual cancer cells in the recipient. * **Hyperacute Rejection:** Rare in BMT compared to solid organs (like Kidney) because BMT is not primarily dependent on pre-formed antibodies against vascular endothelium. **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. [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. 182-183. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 240-241.

Question 240: Which HLA association is seen with Myasthenia gravis?

A. HLA-B27
B. HLA-B51
C. HLA-B47
D. HLA-B8 (Correct Answer)

Explanation: **Explanation:** **Myasthenia Gravis (MG)** is an autoimmune disorder characterized by antibodies against the postsynaptic nicotinic acetylcholine receptors (AChR) at the neuromuscular junction [2]. The correct answer is **HLA-B8**, which is strongly associated with early-onset MG (typically in females under age 40) and is often linked with thymic hyperplasia [1]. * **HLA-B8:** This allele is part of the classic autoimmune haplotype (A1-B8-DR3). Patients with HLA-B8 are predisposed to various autoimmune conditions, including Myasthenia Gravis, Graves' disease, and Celiac disease [1]. * **HLA-B27 (Option A):** This is the most high-yield HLA association in NEET-PG, linked to **Seronegative Spondyloarthropathies** (mnemonic **PAIR**: Psoriatic arthritis, Ankylosing spondylitis, Inflammatory bowel disease-associated arthritis, and Reactive arthritis) [1]. * **HLA-B51 (Option B):** This is specifically associated with **Behçet’s disease**, a systemic vasculitis characterized by recurrent oral and genital ulcers. * **HLA-B47 (Option C):** This allele is associated with **21-hydroxylase deficiency**, the most common cause of Congenital Adrenal Hyperplasia (CAH). **High-Yield Clinical Pearls for NEET-PG:** 1. **Thymic Pathology:** 65-70% of MG patients have thymic hyperplasia (associated with HLA-B8), while 10-15% have a thymoma (usually older patients, no specific HLA association). 2. **Other HLA-DR3 Associations:** While B8 is the Class I association, **HLA-DR3** is the Class II association for MG [1]. 3. **Lambert-Eaton Syndrome:** Often confused with MG, this is a pre-synaptic disorder associated with Small Cell Carcinoma of the Lung and is **not** typically linked to HLA-B8. **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. 49-50. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238.

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Cells and Tissues of the Immune System

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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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