Immunopathology — MCQs

A 20-year-old woman complains of weakness that is worse in the afternoon, worse during prolonged activity, and improved by rest. When fatigued, the patient is unable to hold her head up or chew her food. She often notes diplopia when driving home from work. On physical examination, she has no loss of reflexes, sensation, or coordination. Which of the following is the likely pathogenesis of this disease?

Q347

HLA associated with Rheumatoid arthritis is?

Q348

Human leukocyte antigen (HLA) DR4 occurs in about 70% of patients with rheumatoid arthritis. HLA-DR4 is encoded in the major histocompatibility complex (MHC) region on:

Q349

Rheumatoid factor is directed against ?

Q350

Which of the following statements regarding rejection of solid organ transplants is true?

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 341: A person was brought to the emergency department with facial swelling, itching, and hypotension following a bee sting. The mentioned clinical features are due to the increase in which immunoglobulin?

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

Explanation: IgE - The symptoms of **facial swelling, itching, and hypotension** following a bee sting are characteristic of an immediate hypersensitivity reaction, specifically **anaphylaxis**, which is predominantly mediated by **IgE antibodies** [1]. - **IgE** binds to mast cells and basophils, and upon re-exposure to the allergen (bee venom), triggers the release of potent inflammatory mediators like **histamine**, causing vasodilation, increased vascular permeability, and smooth muscle contraction [1], . *IgG* - **IgG** antibodies are primarily involved in secondary immune responses, conferring long-term immunity, and neutralizing toxins and viruses [1]. - While IgG can be involved in some hypersensitivity reactions (Type II and Type III), it is not the primary immunoglobulin responsible for the acute, systemic symptoms of **anaphylaxis** from a bee sting [1]. *IgA* - **IgA** is the main immunoglobulin found in mucosal secretions, such as those in the gastrointestinal, respiratory, and genitourinary tracts, providing mucosal immunity. - It does not play a significant role in immediate hypersensitivity reactions or the systemic symptoms described in this scenario. *IgM* - **IgM** is the first antibody produced during a primary immune response and is important for activating the complement system and agglutinating antigens [1]. - It is not directly implicated in the pathogenesis of **Type I hypersensitivity reactions** like the anaphylactic response to a bee sting. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-213.

Question 342: Which cell acts as the primary effector cell in type IV (delayed-type) hypersensitivity reactions?

A. Neutrophil
B. Dendritic cell
C. Macrophage (Correct Answer)
D. Cytotoxic T cell

Explanation: ***Macrophage*** - **Macrophages** are the **principal effector cells** in type IV hypersensitivity reactions, responsible for the characteristic tissue damage and inflammation [1]. - They are activated by **IFN-γ and other cytokines** released by sensitized CD4+ Th1 cells upon antigen re-exposure [2]. - Activated macrophages release **inflammatory mediators, lysosomal enzymes, and reactive oxygen species** that cause tissue damage [3]. - They are central to **granuloma formation** (e.g., tuberculosis, sarcoidosis) and the classic tuberculin skin test reaction [1]. *Neutrophil* - **Neutrophils** are the hallmark of acute inflammation and type III hypersensitivity (immune complex reactions). - While neutrophils can be recruited in some type IV reactions (subtype IVd), they are **not the defining effector cells** of classic delayed-type hypersensitivity [1]. *Dendritic cell* - **Dendritic cells** function as **antigen-presenting cells (APCs)** in the sensitization/afferent phase [1]. - They capture and present antigens to naive T cells but do **not serve as effector cells** causing tissue damage in the efferent phase. *Cytotoxic T cell* - **CD8+ cytotoxic T cells** are involved in a specific subtype of type IV hypersensitivity (type IVc) where they directly kill antigen-bearing target cells. - However, in **classic delayed-type hypersensitivity** (type IVa, e.g., tuberculin reaction, contact dermatitis), **macrophages are the predominant effector cells** mediating tissue damage through inflammatory mediators rather than direct cytotoxicity [1]. **Note:** Type IV hypersensitivity is T cell-mediated, with CD4+ Th1 cells initiating the response, but macrophages execute the effector function as the primary tissue-damaging cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Question 343: Which of the following cytokines plays the most crucial role in mediating the inflammatory response and tissue damage in gonococcal arthritis?

A. TNF-α
B. IL-1β (Correct Answer)
C. IL-8
D. IL-6

Explanation: ***IL-1β*** - **IL-1β** is the most crucial cytokine mediating inflammatory response and tissue damage specifically in **gonococcal arthritis** - Neisseria gonorrhoeae infection triggers potent **IL-1β production** through complement activation and bacterial lipooligosaccharide (LOS) [1] - IL-1β drives the production of **matrix metalloproteinases (MMPs)** and other degradative enzymes, leading to **cartilage and bone destruction** - It amplifies the inflammatory cascade by inducing other pro-inflammatory cytokines and chemokines [1] - Experimental models show that **IL-1β blockade significantly reduces joint damage** in gonococcal infections *IL-8* - **IL-8** (CXCL8) is a critical **neutrophil chemokine** that causes the characteristic massive neutrophil infiltration in gonococcal arthritis [1] - While essential for leukocyte recruitment and the purulent synovial fluid seen in this condition, it is primarily a **chemotactic mediator** rather than the main driver of tissue destruction [1] *IL-6* - **IL-6** is a pro-inflammatory cytokine involved in the **acute phase response** and systemic inflammatory features [1] - It contributes to fever, synovitis, and B-cell responses during infection - However, its role in directly mediating joint tissue damage in gonococcal arthritis is **secondary** to IL-1β *TNF-α* - **TNF-α** is a potent pro-inflammatory cytokine important in many forms of arthritis, particularly **rheumatoid arthritis** and chronic inflammatory conditions [1] - While it does contribute to inflammation in septic arthritis, in **gonococcal arthritis specifically**, the cytokine profile is **dominated by IL-1β and IL-8** - The pathophysiology of gonococcal infection differs from other bacterial arthritides where TNF-α may play a more central role **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 97-99.

Question 344: Acute graft rejection occurs within?

A. Few minutes
B. 6-12 months
C. Few hours
D. < 6 months (Correct Answer)

Explanation: ***< 6 months*** - **Acute graft rejection** typically occurs within the first few **weeks to months** after transplantation due to a T-cell mediated immune response against the donor organ [1]. - While it can manifest at any time, the majority of cases occur within the **first 6 months** post-transplant, making this the most appropriate time frame [1]. *Few minutes* - Rejection presenting within minutes of transplantation is characteristic of **hyperacute rejection**, which is caused by pre-existing **donor-specific antibodies** [1]. - This rapid form of rejection is mediated by **complement activation** and leads to immediate graft failure [1]. *6-12 months* - Rejection occurring in this timeframe might still be acute, but the peak incidence is generally earlier. - Rejection presenting after 6 months is often categorized as **late acute rejection** or may start to transition towards signs of chronic rejection, which occurs over a longer period. *Few hours* - Rejection within a few hours could be a very early form of **acute rejection** or a delayed presentation of **hyperacute rejection** [1]. - However, the classic presentation of acute rejection is more prolonged than a few hours, usually developing over days to weeks. **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 345: Rheumatoid factor is an antibody of which class -

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

Explanation: ***IgM*** - **Rheumatoid factor (RF)** is typically an **IgM autoantibody** directed against the Fc region of IgG. - While other isotypes of RF (IgG, IgA) exist, **IgM RF** is the most common form detected in serological tests for **rheumatoid arthritis**. *IgD* - **IgD** antibodies are found in small amounts in the serum and are primarily located on the surface of **B lymphocytes**, where they function as antigen receptors. - They are not associated with autoantibodies like **rheumatoid factor**. *IgE* - **IgE** antibodies are primarily involved in **allergic reactions** and defense against parasites [1]. - High levels of IgE are characteristic of **atopic diseases** such as asthma and allergic rhinitis, not autoimmune conditions like rheumatoid arthritis [1]. *IgG* - While IgG is the most abundant immunoglobulin in serum and plays a crucial role in immune defense, **rheumatoid factor** itself is usually an **IgM or IgA antibody** that targets the Fc portion of IgG. - Therefore, IgG is the *target* of RF often, but **not the isotype of RF itself** in the most common clinical assay. **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.

Question 346: A 20-year-old woman complains of weakness that is worse in the afternoon, worse during prolonged activity, and improved by rest. When fatigued, the patient is unable to hold her head up or chew her food. She often notes diplopia when driving home from work. On physical examination, she has no loss of reflexes, sensation, or coordination. Which of the following is the likely pathogenesis of this disease?

A. Destruction of anterior horn cells by virus
B. Autoantibodies directed against the postsynaptic acetylcholine receptor causing neuromuscular transmission failure (Correct Answer)
C. Demyelinating disease
D. Progressive muscular atrophy caused by spinal degeneration

Explanation: ***Autoantibodies directed against the postsynaptic acetylcholine receptor causing neuromuscular transmission failure*** - The classic presentation of **myasthenia gravis** includes fluctuating weakness that worsens with activity and improves with rest, affecting muscles like those used for **chewing (bulbar weakness)** and **eye movement (diplopia)** [1]. - The underlying pathology is the production of **autoantibodies** that block, alter, or destroy the **nicotinic acetylcholine receptors** at the **postsynaptic membrane** of the neuromuscular junction, leading to impaired signal transmission [1], [2]. *Destruction of anterior horn cells by virus* - This description is characteristic of diseases affecting the **lower motor neurons**, such as **polio** or **spinal muscular atrophy** [3]. - These conditions typically cause **permanent weakness** and **muscle atrophy**, rather than fluctuating weakness that improves with rest, and do not present with diplopia as a primary symptom [3]. *Demyelinating disease* - **Demyelinating diseases**, like **multiple sclerosis**, involve the destruction of the **myelin sheath** around nerves, leading to impaired nerve conduction [4]. - While they can cause weakness and diplopia, the weakness is typically not characterized by the hallmark **fatigability** that improves with rest seen in the patient's presentation [4]. *Progressive muscular atrophy caused by spinal degeneration* - This describes conditions where there is gradual loss of motor neurons, leading to **muscle wasting** and **weakness** [3]. - Unlike the described patient, these diseases typically cause **progressive, constant weakness** and atrophy, without the characteristic diurnal variation and improvement with rest. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 730-731. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 713-714.

Question 347: HLA associated with Rheumatoid arthritis is?

A. HLA-Cw6
B. HLA-DR4 (Correct Answer)
C. HLA-B8
D. HLA-B27

Explanation: ***HLA-DR4*** - **HLA-DR4** is the **MHC Class II allele** most strongly associated with an increased risk and severity of **rheumatoid arthritis**, particularly in populations of European descent [2]. - This association is particularly relevant for the development of antibodies against **citrullinated proteins (ACPAs)**, a hallmark of more aggressive disease [1]. *HLA CW6* - **HLA CW6** is strongly associated with **psoriasis** and **psoriatic arthritis**, not rheumatoid arthritis. - It plays a role in the immune system's response in these conditions, distinct from the autoimmune mechanisms of rheumatoid arthritis. *HLAB8* - **HLA-B8** is associated with several autoimmune diseases, including **celiac disease**, **myasthenia gravis**, and Sjögren's syndrome, but not primarily with rheumatoid arthritis. - It reflects a broader predisposition to autoimmunity rather than a specific link to RA. *HLAB27* - **HLA-B27** is highly associated with **seronegative spondyloarthropathies**, such as **ankylosing spondylitis** and **reactive arthritis** [3]. - Its presence indicates a strong genetic predisposition for these conditions, which differ clinically and immunologically from rheumatoid arthritis [3]. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1212-1214. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1214-1215.

Question 348: Human leukocyte antigen (HLA) DR4 occurs in about 70% of patients with rheumatoid arthritis. HLA-DR4 is encoded in the major histocompatibility complex (MHC) region on:

A. Chromosome 22
B. Chromosome 9
C. Chromosome 18
D. Chromosome 6 (Correct Answer)

Explanation: ***Chromosome 6*** - The HLA complex, an essential part of the **major histocompatibility complex (MHC)**, is located on the **short arm of chromosome 6**. - This region encodes proteins crucial for the immune system's ability to **distinguish self from non-self**, including class I, II, and III MHC molecules [1]. *Chromosome 22* - Chromosome 22 is known for containing genes associated with various conditions but is **not the location of the MHC complex** or HLA genes. - For example, the **BCR gene** involved in the Philadelphia chromosome translocation in chronic myeloid leukemia is found here. *Chromosome 9* - Chromosome 9 harbors genes linked to conditions like **Friedreich's ataxia** and **tuberous sclerosis**, but not the HLA locus. - It also contains genes related to **blood group determination** (ABO system), but not immune recognition via HLA [2]. *Chromosome 18* - Chromosome 18 is associated with several genetic disorders, such as **Edwards syndrome** (trisomy 18), but it is **not where the MHC genes are located**. - Its genes are primarily involved in development and cellular function rather than direct immune surveillance through HLA. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 49-50, 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. 49-50.

Question 349: Rheumatoid factor is directed against ?

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

Explanation: ***IgG*** - **Rheumatoid factor (RF)** is typically an **IgM antibody** that targets the **Fc portion of human IgG**. - This binding leads to the formation of **immune complexes**, which contribute to the inflammation and joint damage seen in **rheumatoid arthritis (RA)** [1]. *IgA* - While IgA can be involved in some autoimmune processes, it is **not the primary target** of rheumatoid factor. - Elevated IgA levels can be seen in various conditions, but **IgA is not the antigen** that RF binds to. *IgM* - **IgM is the class of antibody** that the rheumatoid factor itself usually belongs to (i.e., RF is often an IgM antibody). - However, RF is **not directed against IgM**; it is directed against another immunoglobulin class. *IgD* - **IgD** has a less defined role in the systemic immune response compared to other immunoglobulin classes. - It is **not the target** of rheumatoid factor and is not commonly implicated in the pathogenesis of rheumatoid arthritis in this manner. **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.

Question 350: Which of the following statements regarding rejection of solid organ transplants is true?

A. Most immunosuppressive medications are used to prevent chronic rejection
B. The major cause of graft failure is acute rejection
C. Liver transplants are especially susceptible to hyperacute rejection
D. Hyperacute rejection begins in the operating room with reperfusion of the transplanted organ (Correct Answer)

Explanation: ***Hyperacute rejection begins in the operating room with reperfusion of the transplanted organ*** - **Hyperacute rejection** is a rapidly-occurring immune response that starts almost immediately after the transplanted organ is re-vascularized, often while the patient is still in the operating room [1]. - This type of rejection is mediated by **pre-formed antibodies** (e.g., ABO blood group antibodies or anti-HLA antibodies) in the recipient's circulation that bind to antigens on the donor organ's endothelium, leading to massive thrombosis and organ destruction [1]. *Most immunosuppressive medications are used to prevent chronic rejection* - While immunosuppressants play a role in mitigating **chronic rejection**, their primary and most effective targets are **acute rejection episodes** and the initial prevention of organ rejection [2]. - **Chronic rejection** is often a more complex process involving both immune and non-immune factors, and current immunosuppressive regimens are less effective at completely preventing or reversing it compared to acute rejection. *The major cause of graft failure is acute rejection* - In the long term, **chronic rejection** (or chronic allograft dysfunction) is the leading cause of late graft loss, rather than acute rejection. - With advancements in immunosuppression, **acute rejection rates** have significantly decreased, making chronic issues and non-immune factors more prominent in overall graft failure. *Liver transplants are especially susceptible to hyperacute rejection* - **Liver transplants** are notably more tolerant to ABO and HLA mismatches compared to other solid organ transplants (like kidney or heart). - This relative immunotolerance means that **hyperacute rejection** is far less common in liver transplantation. **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] 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.

Practice by Chapter

Cells and Tissues of the Immune System

Practice Questions

Innate Immunity

Practice Questions

Adaptive Immunity

Practice Questions

Hypersensitivity Reactions

Practice Questions

Autoimmune Diseases

Practice Questions

Immunodeficiency Disorders

Practice Questions

Transplantation Immunopathology

Practice Questions

Immune Response to Infections

Practice Questions

Immunologic Laboratory Techniques

Practice Questions

Tumor Immunology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free