Immunopathology — MCQs
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MHC restriction is a part of all except:
A 45-year-old woman complains of severe headaches and difficulty in swallowing. Over the past 6 months, she has noticed small, red lesions around her mouth as well as thickening of her skin. The patient has "stone facies" on physical examination. Which of the following antigens is the most common and most specific target of autoantibody in patients with this disease?
A 10-year-old boy is brought to the ED after being stung by a bee while playing outside. Within minutes of the sting, he developed shock, respiratory failure, and vascular collapse. What type of hypersensitivity reaction is most likely responsible?
Acute hemolytic blood transfusion reactions are mediated by which type of hypersensitivity reaction?
A skin graft was performed on an immunocompromised patient using tissue from another immunocompromised individual. Weeks later, the patient developed contractures and systemic symptoms. What is the most likely cause?
In Myasthenia gravis, which of the following is the primary target of autoantibodies at the neuromuscular junction?
Which of the following is implicated in the pathogenesis of rheumatoid arthritis?
Transplant rejection does not occur in which of the following conditions?
HLA-mismatched transplant is not a problem in which of the following diseases?
A middle-aged woman presents with dry eyes and dry mouth. Laboratory tests reveal positive anti-Ro (SSA) and anti-La (SSB) antibodies. What is the most likely underlying pathological mechanism?
Immunopathology Indian Medical PG Practice Questions and MCQs
Question 331: MHC restriction is a part of all except:
- A. Antiviral cytotoxic T cell
- B. Antibacterial helper T cell/cytotoxic cells
- C. Allograft rejection
- D. Autoimmune disorder (Correct Answer)
Explanation: **Explanation:** **MHC Restriction** is the process where T cells can only recognize an antigen when it is presented on a specific **Major Histocompatibility Complex (MHC)** molecule. CD8+ T cells are restricted to MHC Class I, while CD4+ T cells are restricted to MHC Class II. **Why "Autoimmune Disorder" is the correct answer:** Autoimmune disorders are characterized by a **failure of self-tolerance** [1]. While MHC alleles (like HLA-B27 or DR4) often predispose an individual to these diseases [2], the pathogenesis involves the immune system attacking self-antigens. In many autoimmune contexts, the damage is mediated by autoantibodies (B-cell mediated) or non-specific inflammatory cytokines where strict MHC restriction is not the defining mechanism of the clinical manifestation, unlike the direct T-cell/Antigen/MHC synapse required for the other options [3]. **Analysis of Incorrect Options:** * **Antiviral Cytotoxic T cells (A):** These are CD8+ cells that *must* recognize viral peptides presented on MHC Class I molecules to kill infected cells. This is a classic example of MHC restriction. * **Antibacterial Helper/Cytotoxic cells (B):** Helper T cells (CD4+) recognize bacterial peptides on MHC Class II (presented by APCs), and Cytotoxic T cells (CD8+) recognize intracellular bacteria on MHC Class I. Both require MHC restriction to function. * **Allograft Rejection (C):** Rejection is driven by the recognition of "nonself" MHC molecules on the donor organ. Whether via the Direct pathway (recognizing donor MHC) or Indirect pathway (donor peptides on recipient MHC), the process is entirely dependent on MHC interaction. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Found on all nucleated cells; presents endogenous antigens to **CD8+** T cells. * **MHC Class II:** Found only on Professional APCs (Dendritic cells, Macrophages, B cells); presents exogenous antigens to **CD4+** T cells. * **Rule of 8:** $1 \times 8 = 8$ (MHC I $\times$ CD8) and $2 \times 4 = 8$ (MHC II $\times$ CD4). * **HLA Linkage:** Remember HLA-B27 (Ankylosing Spondylitis) and HLA-DR4 (Rheumatoid Arthritis) as high-yield associations [2]. **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. 175-176. [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. 177-178. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 219-220.
Question 332: A 45-year-old woman complains of severe headaches and difficulty in swallowing. Over the past 6 months, she has noticed small, red lesions around her mouth as well as thickening of her skin. The patient has "stone facies" on physical examination. Which of the following antigens is the most common and most specific target of autoantibody in patients with this disease?
- A. C-ANCA (anti-proteinase-3)
- B. Double-stranded DNA
- C. P-ANCA (anti-myeloperoxidase)
- D. Scl-70 (anti-topoisomerase I) (Correct Answer)
Explanation: ### Explanation **1. Why the Correct Answer is Right:** The clinical presentation—**thickening of the skin**, **"stone facies"** (loss of facial expression due to skin tightening) [2], and **difficulty swallowing** (esophageal dysmotility)—is classic for **Systemic Sclerosis (Scleroderma)** [1,3]. The "small red lesions" refer to telangiectasias [3]. In the **Diffuse Cutaneous Systemic Sclerosis** subtype, the most specific and high-yield autoantibody is **Anti-Scl-70**, which targets **DNA Topoisomerase I** [1]. This antibody is associated with a higher risk of rapid skin involvement and interstitial lung disease (ILD) [1]. **2. Why the Other Options are Incorrect:** * **A & C (C-ANCA & P-ANCA):** These are markers for **Vasculitides**. C-ANCA (anti-PR3) is highly specific for Granulomatosis with Polyangiitis (Wegener’s), while P-ANCA (anti-MPO) is associated with Microscopic Polyangiitis and Churg-Strauss syndrome. * **B (dsDNA):** This is highly specific for **Systemic Lupus Erythematosus (SLE)** and is often used to monitor disease activity and renal involvement. **3. NEET-PG High-Yield Pearls:** * **Systemic Sclerosis Subtypes:** * **Diffuse:** Anti-Scl-70 (Anti-topoisomerase I). High risk of pulmonary fibrosis [1]. * **Limited (CREST Syndrome):** Anti-Centromere antibody [1]. Better prognosis, but risk of Pulmonary Arterial Hypertension (PAH) [1,3]. * **Pathogenesis:** Characterized by excessive fibrosis due to fibroblast activation and vascular damage (obliterative endarteritis) [1,4]. * **Gastrointestinal:** The esophagus is the most common internal organ involved (lower 2/3rd), leading to "rubber hose" esophagus and dysphagia [3,5]. * **Renal:** "Scleroderma Renal Crisis" is a life-threatening complication treated with ACE inhibitors. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 238-239. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 686-687. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 689-690. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 236-237. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 238.
Question 333: A 10-year-old boy is brought to the ED after being stung by a bee while playing outside. Within minutes of the sting, he developed shock, respiratory failure, and vascular collapse. What type of hypersensitivity reaction is most likely responsible?
- A. A. IgE-mediated reaction (Correct Answer)
- B. D. T cell-mediated response
- C. B. IgG-mediated reaction
- D. C. IgA-mediated hypersensitivity
Explanation: A. IgE-mediated reaction - This is a **Type I hypersensitivity reaction** (anaphylaxis) [2], characterized by the rapid release of potent mediators (like **histamine** and leukotrienes) from mast cells and basophils upon re-exposure to an allergen (bee venom) [1][3][4]. - The clinical presentation of rapid onset **shock**, **respiratory failure**, and **vascular collapse** minutes after exposure is the classic, life-threatening manifestation of systemic anaphylaxis [5]. *B. IgG-mediated reaction* - IgG is the primary mediator in **Type II (cytotoxic)** and **Type III (immune complex)** hypersensitivity reactions, which are typically delayed (hours to days) and not immediate [2]. - Type II reactions involve antibody binding directly to cell surface antigens (e.g., hemolytic anemia), while Type III involves tissue damage from soluble immune complexes (e.g., serum sickness) [2]. *C. IgA-mediated hypersensitivity* - IgA is predominantly found in mucosal secretions and protects mucosal barriers; it is not the main antibody responsible for classic Type I systemic anaphylaxis. - While IgA can be implicated in various disorders (such as **celiac disease**), it does not mediate the massive, immediate systemic degranulation seen in bee sting-induced shock. *D. T cell-mediated response* - This refers to **Type IV hypersensitivity**, which is a **delayed reaction** mediated by sensitized T lymphocytes and macrophages (e.g., contact dermatitis, tuberculin test). - Type IV reactions typically take 24–72 hours to manifest and lack the rapid, humoral-driven vasodilation and bronchospasm characteristic of Type I anaphylaxis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213.
Question 334: Acute hemolytic blood transfusion reactions are mediated by which type of hypersensitivity reaction?
- A. Type I
- B. Type III
- C. Type II (Correct Answer)
- D. Type IV
Explanation: ***Type II***- Acute hemolytic transfusion reactions, the most dangerous type, occur when pre-formed recipient antibodies (usually **IgM** against donor ABO antigens) bind to antigens on the surface of transfused red blood cells, leading to their destruction. [1] - This antibody binding activates the **complement cascade** and/or causes **opsonization** and phagocytosis, characteristic features of Type II hypersensitivity (antibody-mediated cytotoxic reaction). [1], [2] *Type I*- Type I hypersensitivity is **IgE-mediated**, responsible for immediate allergic reactions such as anaphylaxis or urticaria, often due to plasma proteins in the donor blood product. [4] - It involves mast cell and basophil degranulation upon antigen binding, leading to the rapid release of mediators like **histamine**.*Type III*- Type III hypersensitivity involves the formation and deposition of circulating **antigen-antibody immune complexes** in tissues, which then activate complement and cause inflammation (e.g., serum sickness). [3] - While some non-hemolytic transfusion reactions may involve immune complexes, the primary mechanism of cell destruction in acute hemolytic reactions is not due to complex deposition.*Type IV*- Type IV hypersensitivity is a **delayed-type reaction** mediated by **T lymphocytes** and macrophages, taking 24-72 hours or more to manifest. - This mechanism is involved in conditions like graft-versus-host disease (GVHD) and contact dermatitis, but it is not the cause of immediate or acute immunologic transfusion reactions involving red cell destruction. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213.
Question 335: A skin graft was performed on an immunocompromised patient using tissue from another immunocompromised individual. Weeks later, the patient developed contractures and systemic symptoms. What is the most likely cause?
- A. Delayed wound healing
- B. Rejection due to recipient T8 cells
- C. Graft failure
- D. Graft-versus-host disease (Correct Answer)
Explanation: ***Correct: Graft-versus-host disease (GVHD)*** - GVHD occurs when **immunocompetent donor T lymphocytes** from the graft recognize recipient tissues as foreign and mount an immune attack [1] - Key scenario: **Immunocompromised recipient** receiving tissue from another person (even if donor is immunocompromised, donor T cells in the graft can still be functional) - The recipient's compromised immune system **cannot eliminate donor lymphocytes**, allowing them to engraft and attack host tissues [1] - **Contractures** are characteristic of chronic GVHD affecting skin and connective tissue - **Systemic symptoms** (fever, diarrhea, hepatitis) reflect multi-organ involvement typical of GVHD - Timeline of **weeks** fits both acute (2-100 days) and chronic (>100 days) GVHD *Incorrect: Delayed wound healing* - Would present as local wound complications, not systemic symptoms - Does not explain contractures or multi-organ involvement - Typically occurs within days, not weeks *Incorrect: Rejection due to recipient T8 cells* - This describes **host-versus-graft** (rejection), not graft-versus-host - Patient is **immunocompromised**, so recipient T cells are impaired and unlikely to mount effective rejection - Would cause graft loss, not systemic symptoms in the recipient *Incorrect: Graft failure* - Non-specific term that doesn't explain the clinical presentation - Would present as loss of graft function/wound dehiscence, not systemic symptoms - Does not account for contractures or multi-organ disease **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 244-245.
Question 336: In Myasthenia gravis, which of the following is the primary target of autoantibodies at the neuromuscular junction?
- A. Acetylcholinesterase
- B. Voltage-gated calcium channels at NMJ
- C. Presynaptic ACh receptor
- D. Post-synaptic ACh Receptor (Correct Answer)
Explanation: ***Post-synaptic ACh Receptor*** - Myasthenia gravis is an autoimmune disorder where **IgG autoantibodies** are produced against the nicotinic **acetylcholine receptors (AChR)** on the post-synaptic muscle membrane [1], [2]. - These antibodies block acetylcholine from binding and also cause **complement-mediated destruction** and accelerated degradation of the receptors, leading to fatigable muscle weakness [1]. *Presynaptic ACh receptor* - Presynaptic acetylcholine receptors are involved in modulating the release of acetylcholine, but they are not the primary target of autoantibodies in Myasthenia Gravis. - Conditions targeting presynaptic components, like **Lambert-Eaton Myasthenic Syndrome**, involve a different pathophysiology. *Voltage-gated calcium channels at NMJ* - Autoantibodies against presynaptic **P/Q-type voltage-gated calcium channels (VGCCs)** are the hallmark of **Lambert-Eaton Myasthenic Syndrome (LEMS)**, not Myasthenia Gravis. - The blockade of these channels impairs the presynaptic release of acetylcholine, leading to a distinct clinical picture of weakness that often improves with activity. *Acetylcholinesterase* - **Acetylcholinesterase** is the enzyme that breaks down acetylcholine in the synaptic cleft; it is not the target of autoantibodies in this disease [3]. - **Acetylcholinesterase inhibitors**, such as pyridostigmine, are a primary treatment for Myasthenia Gravis because they increase the availability of acetylcholine at the neuromuscular junction [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1238-1239.
Question 337: Which of the following is implicated in the pathogenesis of rheumatoid arthritis?
- A. Defective cellular and humoral immunity
- B. Autoimmunity (Correct Answer)
- C. Chronic microbial infections
- D. IgE mediated
Explanation: ***Autoimmunity*** - **Rheumatoid arthritis (RA)** is fundamentally a chronic, systemic **autoimmune disease** where the immune system attacks the synovium and joint structures [1].- The pathogenesis involves the loss of **self-tolerance**, leading to the production of autoantibodies (like **RF** and **Anti-CCP**) and T-cell mediated chronic inflammation [2]. *IgE mediated*- **IgE mediated** reactions define Type I (Immediate) Hypersensitivity, which is the mechanism behind allergic reactions like **anaphylaxis** and asthma.- RA is primarily driven by Type III (immune complex) and Type IV (T-cell mediated) hypersensitivity mechanisms, not IgE-mediated mast cell degranulation.*Defective cellular and humoral immunity*- RA is characterized by an **overactive and misdirected** immune response against self-antigens, not a broad deficiency in the immune system.- Conditions resulting from defective immunity are classified as **immunodeficiency syndromes**, typically leading to recurrent, severe opportunistic infections.*Chronic microbial infections*- While certain infections may act as an environmental trigger in genetically susceptible individuals (**molecular mimicry**), the persistence of RA is due to established **autoimmunity**, not ongoing microbial proliferation.- Diseases caused by chronic microbial infections, such as **tuberculosis** or **leprosy**, resolve upon successful eradication of the pathogen, unlike RA which requires continuous immunosuppression. **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. 175-176. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212.
Question 338: Transplant rejection does not occur in which of the following conditions?
- A. Bare lymphocyte syndrome
- B. Severe Combined Immunodeficiency (SCID) (Correct Answer)
- C. Chronic granulomatous disease
- D. DiGeorge syndrome
Explanation: The condition of Severe Combined Immunodeficiency (SCID) is characterized by a profound failure of adaptive immunity due to defects in the creation or function of both T-lymphocytes and B-lymphocytes [1]. Transplant rejection is a primarily cell-mediated process dependent on functional T-cells; since SCID recipients lack these critical immune cells, they cannot recognize or attack the donor graft, thus rejection does not occur [1]. Bare lymphocyte syndrome (BLS) is characterized by defective expression of MHC class I or MHC class II molecules, leading to severe immunodeficiency but typically not the complete and absolute absence of T-cell function like SCID. While severely immunocompromised, the mechanisms required for adaptive immunity are present, albeit impaired, and rejection risk is complex, making SCID the more definitive answer. Chronic granulomatous disease (CGD) involves an inherited deficiency of NADPH oxidase in phagocytes, impairing their ability to kill internalized microbes using oxidative burst [2]. CGD affects the innate immune system; the adaptive immune system (T-cells responsible for recognizing the graft) remains fully functional, meaning rejection will occur. DiGeorge syndrome causes variable degrees of T-cell deficiency due to the hypoplasia or aplasia of the thymus resulting from impaired development of the third and fourth pharyngeal pouches [2]. Though T-cell function is impaired, many patients retain residual or partial T-cell immunity, meaning a delayed or mild form of transplant rejection can still occur [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 246-248. [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. 167-168.
Question 339: HLA-mismatched transplant is not a problem in which of the following diseases?
- A. Job's syndrome
- B. Wiskott-Aldrich syndrome
- C. Chediak-Higashi syndrome
- D. Bare lymphocyte syndrome (Correct Answer)
Explanation: **Bare lymphocyte syndrome (Correct)** - **Bare Lymphocyte Syndrome** (BLS) is characterized by a failure to express **MHC Class I (Type I)** or **MHC Class II (Type II)** molecules on the cell surface, crucial for antigen presentation. - The absence of functional MHC in the recipient means their cells cannot effectively present the donor's HLA antigens, minimizing host immune rejection (host-versus-graft rejection) and allowing for the successful use of **HLA-mismatched transplants**. *Wiskott-Aldrich syndrome (Incorrect)* - This X-linked immunodeficiency involves the **WASp gene** and affects the cytoskeleton of hematopoietic cells, leading to defects in **T-cell function** and a high risk of autoimmune disease. - Since the patient's capacity for MHC presentation is generally intact, standard severe **Graft-versus-Host Disease (GvHD)** is a major risk following mismatched transplant, necessitating stringent HLA matching. *Job's syndrome (Incorrect)* - Job's syndrome (Hyper-IgE syndrome) is typically caused by mutations in **STAT3**, impairing signal transduction necessary for Th17 cell differentiation and resulting in defective neutrophil chemotaxis. - This syndrome does not eliminate the ability of the recipient's cells to express and utilize MHC molecules; therefore, an **HLA-matched donor** is required to prevent transplant rejection and GvHD. *Chediak-Higashi syndrome (Incorrect)* - Caused by a mutation in the **LYST gene**, leading to defective lysosomal trafficking, which primarily affects phagocytes and pigment cells. - Although it is an immunodeficiency, the fundamental mechanisms for T-cell recognition of foreign alloantigens (such as mismatched HLA) are functional, making a severe **HLA mismatch** highly problematic and usually fatal.
Question 340: A middle-aged woman presents with dry eyes and dry mouth. Laboratory tests reveal positive anti-Ro (SSA) and anti-La (SSB) antibodies. What is the most likely underlying pathological mechanism?
- A. IgE-mediated hypersensitivity reaction
- B. Lymphocytic infiltration and destruction of salivary and lacrimal glands (Correct Answer)
- C. Destruction of exocrine glands by neutrophils
- D. Deposition of amyloid in salivary glands
Explanation: ***Lymphocytic infiltration and destruction of salivary and lacrimal glands*** - Sjögren's syndrome (suggested by dry eyes, dry mouth, and **anti-Ro/SSA** & **anti-La/SSB** positivity) is pathologically defined by intense focal **lymphocytic infiltration** (primarily CD4+ T cells) within the affected exocrine glands [1]. - This chronic autoimmune damage, also known as focal glandular adenitis, leads to atrophy and functional abolition of the **salivary** and **lacrimal glands**, causing sicca symptoms [2]. *Destruction of exocrine glands by neutrophils* - **Neutrophils** are primarily involved in acute inflammation or bacterial infections; they are not the hallmark destructive cell type in this **chronic autoimmune disease**. - The characteristic lesion in Sjögren's syndrome involves extensive infiltration by **lymphocytes**, not neutrophils [1]. *IgE-mediated hypersensitivity reaction* - This type of reaction (Type I) involves mast cell degranulation and is responsible for **allergic responses** and anaphylaxis, which is clinically and pathologically distinct from Sjögren's syndrome. - Sjögren's syndrome involves **Type IV (cell-mediated)** and **Type III (immune complex)** pathology, evidenced by T-cell infiltration and autoantibodies [1]. *Deposition of amyloid in salivary glands* - **Amyloidosis** causing salivary gland enlargement is a rare cause of xerostomia and is characterized by misfolded protein deposition, not by profound **lymphocytic infiltration**. - The presence of specific autoantibodies (**anti-Ro/SSA, anti-La/SSB**) confirms a diagnosis of Sjögren's syndrome, making amyloidosis highly unlikely [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 234-236. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 749-750.
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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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