Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 391: Which of the following HLA types is most commonly associated with rheumatoid arthritis?

A. HLA DR8
B. HLA DR4 (Correct Answer)
C. HLA DQ1
D. HLA B27

Explanation: ***Correct: HLA DR4*** - **HLA-DR4** is the **most strongly associated HLA type with rheumatoid arthritis** globally and is found in a majority of affected individuals. - This association is primarily with the **"shared epitope" alleles within the HLA-DRB1 locus** (particularly HLA-DRB1*04), contributing to genetic susceptibility and disease severity. - The shared epitope hypothesis explains how specific amino acid sequences in the HLA-DR beta chain increase RA risk. *Incorrect: HLA DR8* - While other HLA-DR types may show minor associations in certain populations or with specific disease manifestations, **DR8 is not the primary or most common association** for rheumatoid arthritis. - Its association, if any, is **significantly weaker** compared to HLA-DR4. *Incorrect: HLA DQ1* - **HLA-DQ1** (also known as HLA-DQB1*05 and DQB1*06) is a class II MHC molecule, but it is **not the primary HLA type associated with rheumatoid arthritis**. - While HLA-DQ genes can contribute to autoimmune disease susceptibility, **HLA-DRB1 alleles, particularly DR4**, have a stronger and more consistent link to RA. *Incorrect: HLA B27* - **HLA-B27** is a well-known genetic marker, but it is **classically associated with seronegative spondyloarthropathies** like ankylosing spondylitis, psoriatic arthritis, and reactive arthritis—**not rheumatoid arthritis**. - Its presence is a strong indicator for conditions characterized by **axial skeletal involvement and enthesitis**, differentiating them from RA, which primarily affects peripheral joints symmetrically.

Question 392: Hypersensitivity pneumonitis is classically an immunologically mediated inflammatory reaction. Which type of hypersensitivity is primarily involved?

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

Explanation: ***Immune complex mediated hypersensitivity*** - Hypersensitivity pneumonitis is indeed primarily characterized by **immune complex-mediated inflammation** in response to inhaled antigens [1][2]. - This condition often leads to a **Type III hypersensitivity reaction**, where immune complexes form and trigger inflammation in the lung tissues [1][2]. *Cell mediated hypersensitivity* - While cell-mediated mechanisms are important in many immune responses, hypersensitivity pneumonitis mainly involves **immune complex formation** [2]. - This type predominantly reflects a **Type III hypersensitivity** rather than the typical **Type IV** attributed to cell-mediated reactions [3], though T-cell mediated reactions may also contribute [2]. *Allergic reaction* - Allergic reactions generally refer to **IgE-mediated hypersensitivity**, which typically involves immediate responses and mast cell activation [3]. - Hypersensitivity pneumonitis is not an **immediate hypersensitivity** but rather a delayed immune response to **chronic antigen exposure** [2]. *Type II hypersensitivity* - Type II hypersensitivity is mediated by **IgG or IgM antibodies** targeting specific cells or tissues, causing cell destruction [3]. - This is **not applicable** to hypersensitivity pneumonitis, which involves **immune complexes** accumulating in response to environmental antigens [1][2]. **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. The Lung, pp. 701-702. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 393: What type of hypersensitivity reaction is primarily associated with allergic rhinitis?

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

Explanation: ***Type I hypersensitivity reaction*** - Allergic rhinitis is a classic example of a **Type I hypersensitivity reaction**, mediated primarily by **IgE antibodies** [1]. - Exposure to allergens triggers mast cell degranulation, releasing **histamine** and other mediators that cause symptoms like sneezing, rhinorrhea, and nasal congestion [2]. *Type II* - **Type II hypersensitivity reactions** involve **IgG or IgM antibodies** targeting antigens on cell surfaces or extracellular matrix, leading to cell lysis or dysfunction [4]. - Examples include **hemolytic anemia** and **Goodpasture syndrome**, which are distinct from allergic rhinitis. *Type III* - **Type III hypersensitivity reactions** involve the formation of **immune complexes** (antigen-antibody complexes) that deposit in tissues, leading to inflammation [4]. - Conditions like **serum sickness** and **lupus nephritis** are examples, not allergic rhinitis. *Type IV* - **Type IV hypersensitivity reactions** are **delayed-type hypersensitivity** reactions mediated by **T lymphocytes**, not antibodies. - Examples include **contact dermatitis** and the **tuberculin skin test**, which manifest much later after antigen exposure [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [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. 171-172. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 394: Histamine in anaphylaxis is secreted by which of the following cells?

A. Mast cells (Correct Answer)
B. B-cells
C. Basophils
D. Macrophages

Explanation: ***Mast cells*** - Mast cells are the primary cells responsible for the secretion of **histamine** during anaphylaxis, leading to rapid allergic responses [2][4]. - They are located in **tissues** and are involved in **immediate hypersensitivity reactions** by releasing various mediators upon activation [1][2]. *Basophils* - While basophils do contain **histamine**, they play a lesser role in acute anaphylaxis as compared to mast cells [1]. - Basophils are more associated with chronic allergic reactions rather than the **immediate release** observed in anaphylaxis [1]. *Macrophages* - Macrophages are primarily involved in **phagocytosis** and immune response but do not secrete significant amounts of histamine. - They release cytokines and other mediators but are not key players in **histamine-dependent** anaphylactic reactions. *B-cells* - B-cells are crucial for the production of **antibodies** but do not secrete histamine at all. - They are involved in **adaptive immunity** and do not play a direct role in **anaphylaxis** mechanisms [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.

Question 395: The hypersensitivity reaction involved in the hyperacute rejection of a renal transplant is:

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

Explanation: ***Type II*** - Hyperacute rejection is primarily mediated by **antibody-mediated mechanisms**, indicative of Type II hypersensitivity [2]. - It involves pre-existing **IgG antibodies** that react against donor renal graft antigen, leading to rapid graft destruction [1]. *Type I* - Type I hypersensitivity is associated with **allergic reactions** involving **IgE antibodies**, not relevant to transplant rejection [2]. - Typically involves conditions like **anaphylaxis** or **asthma**, which are unrelated to hyperacute rejection scenarios. *Type IV* - Type IV hypersensitivity is cell-mediated and typically manifests as **delayed-type hypersensitivity**, not acute rejection. - It involves **T cells** and does not play a role in the immediate immune response seen in hyperacute rejection. *Type III* - Type III hypersensitivity involves the formation of immune complexes, leading to conditions like **serum sickness**, not hyperacute rejection. - This type of reaction is usually more relevant in **chronic inflammatory conditions** rather than immediate transplant rejections. **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. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 396: Delayed hypersensitivity is primarily mediated by:

A. Lymphocytes (Correct Answer)
B. Neutrophils
C. Eosinophils
D. Monocytes

Explanation: ***Lymphocytes*** - Delayed hypersensitivity reactions (Type IV hypersensitivity) are **primarily mediated by T cells** (a type of lymphocyte), specifically CD4+ Th1 cells [1], [2]. - Upon re-exposure to an antigen, sensitized T cells recognize the antigen and release **cytokines** (IFN-γ, TNF-α, IL-2) that activate macrophages and recruit other immune cells, leading to tissue damage [1], [4]. - This is the **defining characteristic** of Type IV hypersensitivity, distinguishing it from antibody-mediated reactions [1], [3]. *Neutrophils* - These are the primary cells involved in **acute inflammation** and phagocytosis of bacteria, characteristic of Type III hypersensitivity and bacterial infections. - While neutrophils may be present at sites of delayed hypersensitivity, they are not the primary mediators of this reaction [2]. *Eosinophils* - Eosinophils are primarily associated with **Type I hypersensitivity** (IgE-mediated allergic reactions) and parasitic infections. - They release toxic granule proteins and inflammatory mediators but are not characteristic of Type IV reactions [1]. *Monocytes* - Monocytes differentiate into **macrophages**, which serve as important effector cells in delayed hypersensitivity after being activated by T cell-derived cytokines [4]. - However, macrophages act as **secondary effectors** responding to T cell signals; the T lymphocytes are the primary mediators that initiate and define the delayed hypersensitivity response [1], [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. 173-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [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. 174-175. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 206.

Question 397: Allograft rejection is an example of which type of hypersensitivity reaction?

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

Explanation: ***Delayed hypersensitivity*** - Allograft rejection primarily involves **T-cell mediated mechanisms** [1][3][5], characteristic of delayed hypersensitivity reactions [1][2]. - This type of reaction occurs days to weeks after exposure, leading to lymphocyte infiltration and tissue damage [1][4]. *Immediate hypersensitivity* - This type is mediated by **IgE antibodies** and occurs rapidly (within minutes) upon exposure to the allergen. - It is exemplified by **anaphylaxis**, which is not related to the T-cell-mediated rejection seen in allografts. *Swartzmans reaction* - This is a form of **opsonization and hypersensitivity** that results in systemic reactions due to previously sensitized antigen. - Unlike allograft rejection, it is not specifically related to transplant rejection mechanisms. *GVHD* - Graft-versus-host disease (GVHD) is a complication where the **graft attacks the host's tissues** as seen in hematopoietic stem cell transplants. - While related to immune responses, it is not the same as allograft rejection, which refers to the host's rejection of the graft. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 240. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 240-241.

Question 398: Which antigen is most critical in initiating graft rejection?

A. DHA
B. Polysaccharide
C. HLA - Antigen (Correct Answer)
D. MHC - molecule

Explanation: ***MHC - molecule*** - The **Major Histocompatibility Complex (MHC)** molecules are critical in presenting **antigens** to T-cells, which initiates the graft rejection process [1]. - MHC molecules play a central role in the **immune response** by determining the compatibility of tissue transplanted between individuals [1]. *HLA - Antigen* - HLA is a part of the **MHC** and represents a group of genes, but it is not the most crucial factor for initiating graft rejection on its own. - HLA typing is significant for compatibility [2], but the overall process of rejection is driven by **MHC** interactions with T-cells [1]. *DHA* - **DHA** does not relate to graft rejection as it is an **omega-3 fatty acid** rather than an immune antigen. - It has no direct involvement in **immune response** or tissue compatibility processes. *Polysaccharide* - Polysaccharides are primarily components of **cell walls** in bacteria and fungi, and are not involved in the rejection of grafts. - They do not activate **T-cells** or engage in the typical mechanisms of **graft rejection** mediated by MHC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-241. [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. 179-180.

Question 399: Which type of hypersensitivity reaction is characterized by immune complex formation?

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

Explanation: ***Type-III*** - Immune complex hypersensitivity reactions involve the formation of **antigen-antibody complexes** that deposit in tissues, leading to inflammation [1]. - This type includes conditions like **systemic lupus erythematosus** and **serum sickness**, characterized by tissue damage due to these complexes [2][3]. *Type-II* - Type-II hypersensitivity is mediated by **IgG or IgM antibodies** that target cell surface antigens, leading to cytotoxic effects. - Examples include **hemolytic anemia** and **Graves' disease**, which do not involve immune complex deposition. *Type-IV* - Type-IV hypersensitivity is a **delayed-type** reaction mediated by **T cells**, not antibodies, responsible for conditions like **contact dermatitis** [4]. - It does not involve the formation of immune complexes, unlike Type-III reactions [1]. *Type-I* - Type-I hypersensitivity is an **immediate allergic reaction** mediated by **IgE antibodies**, resulting in conditions like **asthma** and **anaphylaxis**. - This type is characterized by activation of **mast cells** and **basophils**, distinct from immune complex mechanisms. **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. (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.

Question 400: Ram Devi presented with acute onset of generalized edema, sweating, and urticaria within minutes of eating peanuts. This is most suggestive of:

A. T cell mediated cytotoxicity
B. IgG mediated reaction
C. IgE mediated reaction (Correct Answer)
D. IgA mediated hypersensitivity reaction

Explanation: ***IgE mediated reaction*** - **Generalized edema and sweating** are classic symptoms associated with an IgE mediated hypersensitivity reaction, commonly seen in allergic responses [1][2]. - Often results in **anaphylaxis** or allergic urticaria, which can cause systemic reactions leading to edema [4]. *IgA mediated hypersensitivity reaction* - Primarily involved in **mucosal immunity**; does not typically cause **generalized edema** or sweating. - Conditions like **Celiac disease** may present with gastrointestinal symptoms, not systemic edema. *IgG mediated reaction* - IgG hypersensitivity typically occurs in **delayed-type hypersensitivity** or autoimmune disorders, rather than causing acute systemic symptoms like edema [2]. - Often associated with chronic conditions and would not present with **sweating** as a primary feature. *T cell mediated cytotoxicity* - Involves **CD8+ T cells** targeting and destroying infected or dysfunctional cells; not characterized by **systemic edema** or sweating [3]. - More related to **cell-mediated immunity**, particularly in viral infections or graft rejection, rather than immediate hypersensitivity [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212. [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. 216-218. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213.

Practice by Chapter

Cells and Tissues of the Immune System

Practice Questions

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

Practice Questions

Transplantation Immunopathology

Practice Questions

Immune Response to Infections

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Immunologic Laboratory Techniques

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Tumor Immunology

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