Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 361: 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.

Question 362: A 28-year-old female presents with a rash after using a new cosmetic product. A skin biopsy reveals lymphocytic infiltration around the blood vessels and basal cell vacuolization. Which type of hypersensitivity reaction is most likely involved?

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

Explanation: ***Type IV*** - The histological findings of **lymphocytic infiltration** and **basal cell vacuolization** are classic for a **delayed-type hypersensitivity reaction**, which is mediated by T-cells [1, 5]. - This type of reaction is characteristic of **contact dermatitis**, often triggered by cosmetic products, presenting hours to days after exposure [1, 3]. *Type I* - This involves **IgE antibodies** binding to mast cells, leading to immediate release of histamine and other mediators [3]. - Clinically, it would manifest as **urticaria**, **angioedema**, or **anaphylaxis**, and histologically as edema and eosinophil infiltration, not lymphocytic infiltrate and vacuolization [3, 4]. *Type II* - Involves **IgG** or **IgM antibodies** targeting antigens on cell surfaces, leading to cell destruction, dysfunction, or inflammation [3]. - Examples include **hemolytic anemias** or **Goodpasture syndrome**, and it is not associated with skin rashes from cosmetic products in this manner. *Type III* - Characterized by the formation of **immune complexes** (antigen-antibody) that deposit in tissues, leading to inflammation and tissue damage [3]. - This would typically present as **serum sickness**, **vasculitis**, or **arthus reaction**, and the histological features would include neutrophil infiltration and vasculitis, different from the findings described [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. 173-175. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, p. 1166. [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 363: A patient with chronic granulomatous disease is unable to produce which of the following substances that are necessary for microbial killing?

A. Superoxide anion (Correct Answer)
B. Hydrogen peroxide
C. Nitric oxide
D. Hypochlorous acid

Explanation: ***Superoxide anion*** - **Chronic granulomatous disease (CGD)** is characterized by a defect in **NADPH oxidase**, the enzyme responsible for generating the **superoxide anion (O₂⁻)** from oxygen during the respiratory burst [1]. - The inability to produce superoxide is the **primary enzymatic defect** and represents the initial step that fails in the microbial killing pathway [2]. - This defect impairs the formation of all subsequent **reactive oxygen species (ROS)** that are crucial for microbial killing within phagocytes. *Hydrogen peroxide* - **Hydrogen peroxide (H₂O₂)** is generated from the superoxide anion by **superoxide dismutase (SOD)** [1]. - While patients with CGD also cannot effectively produce hydrogen peroxide (since it requires superoxide as a substrate), the **primary enzymatic defect** is at the level of superoxide generation. - Hydrogen peroxide represents a downstream consequence of the superoxide deficiency. *Nitric oxide* - **Nitric oxide (NO)** is produced by **nitric oxide synthase (NOS)** in macrophages via conversion of arginine to citrulline [2]. - This pathway is **independent** of NADPH oxidase and remains **intact in CGD**. - NO production is generally *not* impaired in CGD patients. *Hypochlorous acid* - **Hypochlorous acid (HOCl)** is produced by **myeloperoxidase (MPO)** from hydrogen peroxide and chloride ions [2]. - Like hydrogen peroxide, its production is impaired in CGD as a downstream consequence of the inability to generate the initial superoxide anion. - The **direct enzymatic defect** in CGD is at the NADPH oxidase level, making superoxide the primary substance that cannot be produced. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 59. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91.

Question 364: The primary defect in chronic granulomatous disease (CGD) is:

A. Job's disease
B. Defective H2O2 production (Correct Answer)
C. Defective phagocytosis
D. Myeloperoxidase deficiency

Explanation: ***Defective H2O2 production*** - Chronic granulomatous disease (CGD) is a primary immunodeficiency characterized by the inability of phagocytes (neutrophils, macrophages) to produce **reactive oxygen species**, specifically **superoxide** and its derivatives like H2O2. - This defect is primarily due to mutations in genes encoding components of the **NADPH oxidase enzyme complex**, which is crucial for the **oxidative burst** leading to H2O2 and other antimicrobial agents. *Defective phagocytosis* - Defective phagocytosis refers to an impairment in the engulfment of pathogens, which is not the primary defect in CGD. - In CGD, phagocytes can engulf pathogens, but they cannot effectively kill them intracellularly due to the lack of an **oxidative burst**. *Job's disease* - Job's disease, also known as **hyper-IgE syndrome**, is characterized by high IgE levels, recurrent skin and pulmonary infections, and distinctive facial features. - It is caused by genetic defects in the **STAT3 pathway**, which affects immune cell differentiation and function, and does not involve a primary defect in H2O2 production. *Myeloperoxidase deficiency* - Myeloperoxidase (MPO) deficiency is a condition where neutrophils lack the enzyme **myeloperoxidase**, which contributes to the formation of hypochlorous acid (HOCl) from H2O2 and chloride ions. - While MPO is involved in microbial killing, its deficiency is generally less severe than CGD, as other mechanisms (like H2O2 itself) can still kill pathogens; CGD has a more profound defect in the initial production of ROS.

Question 365: Which type of hypersensitivity reaction is mediated by complement?

A. Type I hypersensitivity
B. Type II hypersensitivity (Correct Answer)
C. No hypersensitivity reaction
D. Type IV hypersensitivity

Explanation: ***Type -2 hypersensitivity*** [1][2] - This type of hypersensitivity involves **IgG or IgM antibodies** binding to antigens on cell surfaces, activating the **complement system**, and mediating cell lysis [1][2]. - It is associated with conditions like **hemolytic anemia** and **Goodpasture syndrome** due to complement activation [1]. *None* - This option suggests there is no complement-mediated hypersensitivity, which contradicts established immunological classifications [2]. - Complement activation is specifically linked to **Type-2 hypersensitivity reactions**, making this option incorrect [1][2]. *Type -4 hypersensitivity* - This is a **T-cell mediated** hypersensitivity, not involving antibodies or complement, making it inappropriate for the question regarding complement-mediated reactions [2]. - Characteristic conditions include **granulomatous diseases** and **contact dermatitis**, distinguishing it from Type-2 hypersensitivity. *Type -1 hypersensitivity* - Type-1 hypersensitivity is primarily **IgE mediated**, involving mast cells and histamine release, without direct involvement of the complement system [2]. - Conditions like **asthma** and **allergic rhinitis** are examples, further separating it from complement-mediated mechanisms [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [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 366: Which of the following is a T-cell mediated disease?

A. Allergic Rhinitis
B. Graves' Disease
C. Systemic Lupus Erythematosus (SLE)
D. Sarcoidosis (Correct Answer)

Explanation: ***Sarcoidosis*** - Sarcoidosis is characterized by the formation of **non-caseating granulomas**, primarily driven by **T-cell accumulation** and activation [1]. - The immune response involves **Th1 lymphocytes** releasing cytokines like **IFN-γ** and **TNF-α**, which promote granuloma formation. *Allergic Rhinitis* - This is a **Type I hypersensitivity reaction** mediated primarily by **IgE antibodies** and **mast cell degranulation**. - While T-cells play a role in orchestrating the IgE response, the immediate symptoms are due to **histamine release**, not direct T-cell cytotoxicity or granuloma formation. *Graves' Disease* - Graves' disease is an **autoimmune disorder** primarily mediated by **autoantibodies** (specifically **thyroid-stimulating immunoglobulins**) that bind to and activate the **TSH receptor**. - Although T-cells are involved in breaking tolerance and supporting B-cell activation, the direct tissue damage and functional changes are antibody-driven. *Systemic Lupus Erythematosus (SLE)* - SLE is a classic **autoimmune disease** characterized by the production of numerous **autoantibodies** (e.g., antinuclear antibodies, anti-dsDNA antibodies) that form **immune complexes**. - These immune complexes deposit in various tissues, leading to inflammation and damage, making it primarily a **Type III hypersensitivity** reaction, heavily B-cell and antibody-mediated. **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. 198-200.

Question 367: Which HLA marker is associated with an increased risk of developing type 1 diabetes mellitus?

A. HLA-B7
B. HLA-DQ3
C. HLA-DQ4
D. HLA-DR4 (Correct Answer)

Explanation: ***DR 4*** - The **HLA-DR4** allele is strongly associated with increased susceptibility to **type 1 diabetes mellitus** [1]. - It plays a crucial role in the **immune response**, promoting autoimmunity against pancreatic beta cells. *B 7* - HLA-B7 is not specifically linked to **type 1 diabetes**, but is more associated with other **autoimmune diseases** like **ankylosing spondylitis**. - It does not show the same level of genetic correlation with **insulin-dependent diabetes** as DR4 does. *DQ 4* - HLA-DQ4 is not the primary marker for **type 1 diabetes**; instead, HLA-DQ2 and DQ8 are more relevant in conditions like **celiac disease**. - Its presence does not have a significant relationship with the autoimmune destruction of **beta cells** in diabetes. *DQ 3* - HLA-DQ3 is less frequently associated with **type 1 diabetes** compared to HLA-DR4 [1]. - It is more involved with other **autoimmune conditions** and does not reflect the same risk for developing diabetes mellitus. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1113.

Question 368: What is the purpose of the Direct Coombs' test?

A. Detection of immune components in the serum.
B. Detection of cell surface antigens on red blood cells (RBCs).
C. Detection of antigens circulating in the serum.
D. Detection of immune components bound to red blood cells (RBCs). (Correct Answer)

Explanation: ***Detection of immune components bound to red blood cells (RBCs).*** - The **Direct Coombs' test** (also known as the direct antiglobulin test or DAT) is used to detect antibodies or complement proteins already bound directly to the surface of **red blood cells (RBCs)** in a patient's body. - This test is crucial for diagnosing autoimmune hemolytic anemia, hemolytic disease of the newborn, and drug-induced hemolysis. *Detection of immune components in the serum.* - This describes the **Indirect Coombs' test** (or indirect antiglobulin test), which detects unbound antibodies circulating in the serum, not those already attached to RBCs. - The indirect Coombs test is typically used for cross-matching blood prior to transfusion or for prenatal screening for atypical antibodies. *Detection of cell surface antigens on red blood cells (RBCs).* - While antigens are present on RBCs, the Direct Coombs' test specifically looks for *bound immune components* (antibodies/complement) on these antigens, not the antigens themselves. - Blood typing tests are used to determine specific cell surface antigens (e.g., ABO, Rh). *Detection of antigens circulating in the serum.* - The Direct Coombs' test focuses on immune components bound to cells, not free-floating antigens in the serum. - Detecting circulating antigens would involve different immunodiagnostic techniques, such as ELISA for specific viral or bacterial antigens.

Question 369: Which cells are responsible for GVHD?

A. Immunocompetent NK cell recipient
B. Immunocompetent T cell donor (Correct Answer)
C. Immunocompetent B cell recipient
D. Immunocompetent T cell recipient

Explanation: ***Immunocompetent T cell donor*** - **Graft-versus-host disease (GVHD)** primarily involves **donor T cells** recognizing the recipient's tissues as foreign. - These donor T cells then mount an immune response against the **host's antigens**, leading to tissue damage. *Immunocompetent B cell recipient* - **B cells** are mostly responsible for **humoral immunity** (antibody production), which is not the primary mechanism of GVHD. - While recipient B cells can contribute to immune responses, they are not the main effector cells in initiating and perpetuating GVHD. *Immunocompetent NK cell recipient* - **Natural killer (NK) cells** are part of the innate immune system and can kill target cells without prior sensitization. - However, recipient NK cells are typically suppressed in the transplant setting and do not mediate GVHD; rather, **donor NK cells** can sometimes have a protective role. *Immunocompetent T cell recipient* - The recipient's immune system, including **recipient T cells**, is usually **immunosuppressed** or ablated before transplantation to prevent graft rejection. - If the recipient's T cells were immunocompetent, they would likely reject the graft, leading to **graft rejection (host-versus-graft reaction)**, which is the opposite of GVHD.

Question 370: Which type of hypersensitivity is characteristically associated with atopic conditions?

A. Local type II hypersensitivity (e.g., Goodpasture syndrome)
B. Systemic type II hypersensitivity (e.g., autoimmune hemolytic anemia)
C. Systemic type I hypersensitivity (e.g., anaphylaxis)
D. Local type I hypersensitivity (e.g., allergic rhinitis, eczema) (Correct Answer)

Explanation: ***Local type I hypersensitivity*** - Atopy refers to a **predisposition** to develop allergic reactions, primarily mediated by **IgE** in response to environmental allergens [1]. - Local type I hypersensitivity includes conditions like **asthma**, **hay fever**, and **eczema**, which are characterized by localized allergic responses [1,2]. *Systemic type II hypersensitivity* - Involves **IgG or IgM antibodies** targeting cell surface antigens, leading to systemic reactions like **hemolytic anemia** or **autoimmune diseases** [2]. - This type does not relate to **immediate hypersensitivity responses** seen in atopic conditions. *Systemic type I hypersensitivity* - Characterized by an **immediate systemic reaction**, such as **anaphylaxis**, which is different from localized allergic responses [2]. - Atopy is primarily associated with local reactions, not systemic hypersensitivity reactions. *Local type II hypersensitivity* - Involves **antibody-mediated damage** to tissues and is associated with conditions like **Graves' disease** and **myasthenia gravis** [2]. - It does not include the localized allergic phenomena typical of atopy, which is mediated by **IgE** [1]. **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. 171-172. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

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Cells and Tissues of the Immune System

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Innate Immunity

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Autoimmune Diseases

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Immunodeficiency Disorders

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Tumor Immunology

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