Immunopathology Practice Questions

Q: Rheumatoid factor is mainly-

IgM. ***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.

Q: Rose-Waaler test is?

Passive agglutination for rheumatoid arthritis. ***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.

Q: Hyperacute rejection occurs within:-

Minutes to hours. ***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.

Q: Which of the following is the most important infiltrate in rheumatoid arthritis?

Macrophages. ***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.

Q: Gene not involved in SCID:

BTK. ***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.

Q: Which type of hypersensitivity is most commonly involved in immediate allergic reactions to penicillin?

Type I. ***Type I*** - Allergic reactions to **penicillin** are primarily mediated by **IgE antibodies** binding to mast cells and basophils [1]. - This binding triggers the release of **histamine** and other inflammatory mediators, leading to symptoms like urticaria, angioedema, and anaphylaxis [2]. *Type II* - This type involves **IgG** or **IgM antibodies** binding to antigens on the surface of host cells, leading to **cell lysis** through complement activation or antibody-dependent cellular cytotoxicity [1]. - While penicillin can rarely cause drug-induced hemolytic anemia (a Type II reaction), the classic allergic reaction is not primarily Type II. *Type III* - Type III hypersensitivity involves the formation of **immune complexes** (antigen-antibody complexes) that deposit in tissues, activating complement and causing inflammation [1]. - This is seen in conditions like **serum sickness** or **Arthus reactions**, which are less common with penicillin allergies and involve different mechanisms. *Type IV* - This is a **delayed-type hypersensitivity reaction** mediated by **T lymphocytes** rather than antibodies, typically occurring 24-72 hours after exposure. - Examples include contact dermatitis (e.g., to poison ivy) or the tuberculin skin test, which are distinct from the immediate IgE-mediated response to penicillin. **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, pp. 211-212.

Question 1

Rheumatoid factor is mainly-

Accepted Answer

IgM

Answer

IgG

Answer

IgD

Answer

IgA

Question 2

Rose-Waaler test is?

Accepted Answer

Passive agglutination for rheumatoid arthritis

Answer

Active agglutination for rheumatoid arthritis

Answer

Active agglutination for rheumatic fever

Answer

Passive agglutination for rheumatic fever

Question 3

All are true about autoimmune disease except:

Accepted Answer

Higher incidence among males

Answer

T cells recognize self-antigen

Answer

Polyclonal B cell activation

Answer

Hashimoto's thyroiditis is an example

Question 4

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

Accepted Answer

CD4+ helper cells

Answer

Lymphocyte

Answer

Macrophages

Answer

Dendritic cells

Question 5

Hyperacute rejection occurs within:-

Accepted Answer

Minutes to hours

Answer

12 hours

Answer

24 hours

Answer

6 hours

Question 6

Which of the following is the most important infiltrate in rheumatoid arthritis?

Accepted Answer

Macrophages

Answer

Dendritic cells

Answer

CD4+ Helper cells

Answer

Neutrophils

Question 7

Gene not involved in SCID:

Accepted Answer

BTK

Answer

ZAP70

Answer

IL2RG

Answer

JAK3

Question 8

Serum sickness is mediated by which type of hypersensitivity?

Accepted Answer

Type III

Answer

Type II

Answer

Type IV

Answer

Type I

Question 9

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

Accepted Answer

Type IV

Answer

Type I

Answer

Type II

Answer

Type III

Question 10

Which type of hypersensitivity is most commonly involved in immediate allergic reactions to penicillin?

Accepted Answer

Type I

Answer

Type II

Answer

Type III

Answer

Type IV

Immunopathology — MCQs

Immunopathology — MCQs

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