Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 351: Rheumatoid factor is mainly-

A. IgG
B. IgD
C. IgM (Correct Answer)
D. IgA

Explanation: ***IgM*** - **Rheumatoid factor (RF)** is primarily an **IgM antibody** that targets the Fc portion of human IgG. While other isotypes (IgA, IgG) can also act as RF, the classic laboratory test predominantly detects **IgM-RF**. [2] *IgG* - Although IgG is the target of rheumatoid factor, the rheumatoid factor itself is **not typically an IgG antibody**. [1] - IgG rheumatoid factors do exist but are **less common** than IgM rheumatoid factors and generally not the primary antigen detected in standard RF assays. *IgD* - **IgD antibodies** are found in very small amounts in the serum and their primary role is largely unknown, though they are involved in B cell activation. - IgD is **not a common isotype** for rheumatoid factor and plays a negligible role in its pathogenesis or detection. *IgA* - **IgA rheumatoid factors** can be present in some patients with rheumatoid arthritis, and their presence may correlate with more severe disease. - However, **IgA-RF is less prevalent** than IgM-RF and is not the main type of antibody measured in standard RF tests. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212. [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. 154-155.

Question 352: Rose-Waaler test is?

A. Active agglutination for rheumatoid arthritis
B. Active agglutination for rheumatic fever
C. Passive agglutination for rheumatoid arthritis (Correct Answer)
D. Passive agglutination for rheumatic fever

Explanation: ***Passive agglutination for rheumatoid arthritis*** - The **Rose-Waaler test** detects **rheumatoid factor (RF)**, a type of autoantibody, using **sheep red blood cells** coated with rabbit IgG. - It is a **passive agglutination** method, meaning that the antigen (rabbit IgG) is adsorbed onto an inert particle (sheep red blood cells). *Active agglutination for rheumatoid arthritis* - This description is incorrect because the Rose-Waaler test uses **antigen-coated particles** (passive), rather than directly agglutinating the rheumatoid factor for detection (active). - **Active agglutination** (e.g., direct bacterial agglutination) involves antibodies directly binding to and clumping antigens that are naturally present on or within cells. *Active agglutination for rheumatic fever* - Rheumatic fever is diagnosed based on **clinical criteria** (Jones criteria) and evidence of recent **Streptococcus pyogenes infection**, not directly by an agglutination test for rheumatic fever itself. - The **Rose-Waaler test** is specifically for **rheumatoid factor**, associated with rheumatoid arthritis, not rheumatic fever [1]. *Passive agglutination for rheumatic fever* - Although it's a **passive agglutination** test, the **Rose-Waaler test** is designed to detect **rheumatoid factor** (RF) in serum, which is a hallmark of **rheumatoid arthritis** [1]. - Rheumatic fever diagnosis involves tests like **ASO titer** or anti-DNase B, which are also antibody detection tests but against streptococcal antigens, not rheumatoid factor, and may not be classified as passive agglutination in the same manner. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1212-1214.

Question 353: All are true about autoimmune disease except:

A. Higher incidence among males (Correct Answer)
B. T cells recognize self-antigen
C. Polyclonal B cell activation
D. Hashimoto's thyroiditis is an example

Explanation: ***Higher incidence among males*** - Autoimmune diseases (Ads) generally have a **higher incidence among females** than males, challenging the statement that they are more common in males [1]. - For example, conditions like **Systemic Lupus Erythematosus (SLE)** and **Rheumatoid Arthritis (RA)** show a pronounced female predominance [1]. *T cells recognize self-antigen* - This statement is true; in autoimmune diseases, **autoreactive T cells** fail to undergo proper selection and differentiation, leading them to recognize and attack **self-antigens** [2]. - This recognition often mediates tissue damage, as seen in **Type 1 Diabetes** where T cells target pancreatic beta cells [2]. *Polyclonal B cell activation* - This is also true; autoimmune diseases often involve **polyclonal B cell activation**, leading to the production of various **autoantibodies** that target self-components. - This broad activation contributes to the diverse clinical manifestations and systemic nature of many autoimmune conditions like **Systemic Lupus Erythematosus**. *Hashimoto's thyroiditis is an example* - This statement is true; **Hashimoto's thyroiditis** is a classic example of an **organ-specific autoimmune disease** where autoantibodies and autoreactive T-cells attack thyroid gland components [3]. - It results in **hypothyroidism** due to chronic inflammation and gradual destruction of thyroid follicles [3]. **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. 175-178. [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. 176-177. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1089-1090.

Question 354: In rheumatoid arthritis, which type of cells are prominently involved in the pathogenesis?

A. Lymphocyte
B. Macrophages
C. CD4+ helper cells (Correct Answer)
D. Dendritic cells

Explanation: ***CD4+ helper cells*** - **CD4+ helper T cells** are the most prominently involved cells in the pathogenesis of rheumatoid arthritis, orchestrating the chronic inflammatory cascade through production of **pro-inflammatory cytokines** (TNF-α, IL-17, IFN-γ) [4, 5]. - These cells activate **B cells** (leading to autoantibody production including RF and anti-CCP), **macrophages**, and **synovial fibroblasts**, resulting in sustained inflammation and joint destruction [1]. - The **synovial membrane** in RA shows prominent T-cell infiltration, and the disease responds to **T-cell targeted therapies**, confirming their central pathogenic role [2]. *Macrophages* - While **macrophages** are numerically abundant in the rheumatoid synovium and contribute significantly to inflammation by producing **TNF-α, IL-1, and IL-6**, their activation is largely **dependent on T-cell signals** [1]. - They act as effector cells downstream of T-cell activation rather than being the primary drivers of the disease process. *Lymphocyte* - This is a **broad category** encompassing both T cells and B cells, making it less specific than identifying the particular subset (CD4+ T cells) most critical to RA pathogenesis [3]. - While technically correct that lymphocytes are involved, the more precise answer identifies the specific T-cell subset. *Dendritic cells* - **Dendritic cells** serve as **antigen-presenting cells** that initiate the immune response by presenting self-antigens to T cells in RA [4, 5]. - However, they function primarily in the **initiation phase** rather than being prominently involved throughout the sustained chronic inflammatory process that characterizes established RA. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 223-224. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1212-1214. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218.

Question 355: Hyperacute rejection occurs within:-

A. 12 hours
B. 24 hours
C. 6 hours
D. Minutes to hours (Correct Answer)

Explanation: ***Minutes to hours*** - **Hyperacute rejection** is a rapidly occurring complication post-transplant, characterized by its onset within minutes to hours after **organ reperfusion** [1]. - This type of rejection is mediated by pre-formed **recipient antibodies** that recognize donor antigens, leading to immediate graft damage [1]. *12 hours* - While plausible, 12 hours is a bit too broad as **hyperacute rejection** primarily begins much sooner, typically within the first few hours [1]. - This timeframe might overlap with the initial stages of **acute cellular rejection**, which typically occurs days to weeks later [1]. *24 hours* - **Hyperacute rejection** is almost always observed and causes graft failure well before the 24-hour mark, if it is going to happen. - Rejection occurring within this extended period is more indicative of **accelerated acute rejection** rather than true hyperacute rejection. *6 hours* - While hyperacute rejection certainly can occur within 6 hours, "minutes to hours" better captures the immediate onset, often within seconds or minutes [1]. - Some cases of **hyperacute rejection** can be so rapid that the 6-hour mark would be considered a late presentation. **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 356: Which of the following is the most important infiltrate in rheumatoid arthritis?

A. Dendritic cells
B. CD4+ Helper cells
C. Macrophages (Correct Answer)
D. Neutrophils

Explanation: ***Macrophages*** - **Macrophages** are crucial in rheumatoid arthritis synovium due to their role in producing **pro-inflammatory cytokines** like TNF-̑, IL-1, and IL-6, which drive joint destruction [1], [2]. - They also contribute to the **pannus formation** and degrade cartilage and bone through the release of proteases [1]. *Dendritic cells* - While present in the synovium, **dendritic cells primarily function as antigen-presenting cells**, initiating T-cell responses. - Their direct contribution to tissue damage and chronic inflammation is less prominent than that of macrophages. *CD4+ Helper cells* - **CD4+ T helper cells** orchestrate the immune response by activating B cells and macrophages, but they are not the primary effector cells causing direct tissue damage [3]. - They secrete cytokines that promote inflammation but do not directly participate in tissue degradation. *Neutrophils* - **Neutrophils are abundant in the synovial fluid** during acute flares, contributing to inflammation and breakdown of cartilage through the release of enzymes. - However, their role in the chronic, sustained synovial inflammation and tissue destruction characteristic of RA is less significant compared to macrophages. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212.

Question 357: Gene not involved in SCID:

A. BTK (Correct Answer)
B. ZAP70
C. IL2RG
D. JAK3

Explanation: ***BTK*** - **Bruton's tyrosine kinase (BTK)** is associated with **X-linked agammaglobulinemia (XLA)**, a primary immunodeficiency characterized by the absence of mature B cells and significantly reduced antibody production. While it causes severe immune deficiency, it is not a direct cause of **SCID**. - XLA results in recurrent bacterial infections due to an inability to produce antibodies, rather than the severe combined T and B cell dysfunction seen in SCID. *ZAP70* - **ZAP70** deficiency is a cause of **SCID**. It leads to impaired T-cell receptor signaling, resulting in profound functional T-cell lymphopenia. - Patients with ZAP70 deficiency have normal numbers of CD4 T cells but very low or absent CD8 T cells, and their T cells are functionally impaired, leading to severe immunodeficiency. *IL2RG* - The **IL2RG** gene encodes the common gamma chain (γc), a crucial component of several **interleukin receptors (IL-2, IL-4, IL-7, IL-9, IL-15, IL-21)**. [1] - Mutations in IL2RG cause **X-linked SCID (X-SCID)**, the most common form of SCID, leading to a block in T-cell and NK-cell development due to defective cytokine signaling. [1] *JAK3* - **Janus kinase 3 (JAK3)** is a tyrosine kinase that associates with the **common gamma chain (γc)** and is essential for cytokine signaling downstream of the γc-containing receptors. [1] - **JAK3 deficiency** results in an **autosomal recessive form of SCID**, clinically indistinguishable from X-SCID, with impaired T-cell and NK-cell development due to defective cytokine signaling. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 247-248.

Question 358: Serum sickness is mediated by which type of hypersensitivity?

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

Explanation: ***Type III*** - Serum sickness is a classic example of a **Type III hypersensitivity reaction**, characterized by the formation of **immune complexes** [1], [2]. - These immune complexes deposit in various tissues (e.g., blood vessels, joints, kidneys), leading to inflammation and tissue damage [3]. *Type II* - **Type II hypersensitivity** involves antibodies (IgG or IgM) binding directly to antigens on the surface of cells or in the extracellular matrix, leading to cell lysis or dysfunction. - Examples include **hemolytic transfusion reactions** or autoimmune hemolytic anemia, which are distinct from serum sickness. *Type IV* - **Type IV hypersensitivity** is a **delayed-type hypersensitivity (DTH)** reaction mediated by T cells rather than antibodies. - It typically manifests 24-72 hours after antigen exposure and is seen in conditions like **contact dermatitis** or tuberculosis skin tests. *Type I* - **Type I hypersensitivity** is an immediate reaction mediated by **IgE antibodies** binding to mast cells and basophils, leading to the release of inflammatory mediators upon re-exposure to an allergen. - Examples include **anaphylaxis** or allergic rhinitis, which have a rapid onset and different underlying mechanisms compared to serum sickness. **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] 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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.

Question 359: Which type of hypersensitivity reaction is involved in allergic contact dermatitis?

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

Explanation: ***Type IV*** - Allergic contact dermatitis is a classic example of a **Type IV hypersensitivity reaction**, also known as **delayed-type hypersensitivity** [2]. - It is mediated by **T-cells** that recognize antigens presented on antigen-presenting cells, leading to inflammation typically 24-72 hours after exposure [1], [4]. *Type I* - **Type I hypersensitivity** is an immediate reaction mediated by **IgE antibodies** binding to mast cells and basophils, leading to histamine release [3]. - Examples include **anaphylaxis** and **allergic rhinitis**, which manifest rapidly after exposure, unlike allergic contact dermatitis. *Type II* - **Type II hypersensitivity** involves **IgG or IgM antibodies** targeting antigens on cell surfaces, leading to cell destruction or dysfunction [3]. - Examples include **hemolytic anemia** or **Goodpasture's syndrome**, which are distinct from contact dermatitis. *Type III* - **Type III hypersensitivity** involves the formation and deposition of **immune complexes** (antigen-antibody complexes) in tissues, leading to inflammation and tissue damage [3]. - Examples include **serum sickness** and **lupus nephritis**, which present differently from skin contact reactions. **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. 173-174. [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. 174-175. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 218.

Question 360: In a patient with a history of organ transplantation, which type of hypersensitivity reaction is primarily responsible for graft rejection that occurs days to weeks after transplantation?

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

Explanation: Type IV hypersensitivity - This is a **delayed-type hypersensitivity** reaction, primarily mediated by **T-cells** and macrophages, which is characteristic of acute graft rejection occurring days to weeks post-transplantation [3]. - **Cytotoxic T lymphocytes (CTLs)** directly recognize and kill foreign graft cells, while helper T cells activate macrophages, leading to inflammation and tissue damage in the transplanted organ [2], [4]. Type I hypersensitivity - This is an **immediate hypersensitivity** reaction mediated by **IgE antibodies** and mast cells, typically causing allergic reactions like asthma or anaphylaxis. - It does not play a significant role in typical graft rejection, which is a cell-mediated response to foreign antigens. Type II hypersensitivity - This involves **antibody-mediated cytotoxicity** where antibodies target self-antigens on cell surfaces or extracellular matrix, leading to cell lysis. - While Type II hypersensitivity can contribute to **hyperacute rejection** (occurring minutes to hours post-transplant due to pre-formed antibodies), it is not the primary mechanism for graft rejection occurring days to weeks later [3]. Type III hypersensitivity - This reaction involves the formation of **immune complexes** (antigen-antibody complexes) that deposit in tissues, leading to inflammation and tissue damage [1]. - While immune complexes can contribute to some forms of chronic rejection, they are not the primary mechanism responsible for **acute graft rejection** that occurs days to weeks after transplantation. **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. 173-174. [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. 180-181. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 240.

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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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