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PCB 3233 Exam 4 V2 | PCB 3233 Immunology | Actual Q&A with Rationale (PCB3233 Exam 4) | University of Central Florida

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PCB 3233 Exam 4 V2 | PCB 3233 Immunology | Actual Q&A with Rationale (PCB3233 Exam 4) | University of Central Florida

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PCB 3233 Exam 4 V2 | PCB 3233
Immunology | Actual Q&A with Rationale
(PCB3233 Exam 4) | University of Central
Florida
1. Which immunoglobulin isotype is the primary mediator of Type I hypersensitivity

reactions?

A. IgG


B. IgE


C. IgM


D. IgA


Answer: B


Rationale: IgE is the specific antibody responsible for immediate hypersensitivity

reactions by binding to FceRI receptors on mast cells and basophils. Upon cross-linking by

an allergen, these cells degranulate and release vasoactive amines like histamine. This

isotype is typically found at very low levels in the serum compared to IgG but is potent in

triggering allergic responses.


2. In the context of Type II hypersensitivity, which mechanism leads to the destruction of

target cells?

A. Complement-mediated lysis or Antibody-Dependent Cell-mediated Cytotoxicity (ADCC)

,B. Immune complex deposition in small vessels


C. Delayed-type hypersensitivity mediated by Th1 cells


D. Degranulation of eosinophils via IgE binding


Answer: A


Rationale: Type II hypersensitivity involves IgG or IgM antibodies binding to antigens on

the surface of specific cells or tissues. This binding can activate the classical complement

pathway, leading to the formation of the membrane attack complex. Additionally, it can

recruit NK cells or macrophages to destroy the target cell through ADCC mechanisms.


3. Systemic Lupus Erythematosus (SLE) is characterized by the deposition of immune

complexes, making it which type of hypersensitivity?

A. Type I


B. Type III


C. Type II


D. Type IV


Answer: B


Rationale: Type III hypersensitivity is defined by the formation of small, soluble antigen-

antibody complexes that are not effectively cleared from the circulation. These complexes

deposit in basement membranes of various organs, such as the kidneys and joints, where

they trigger inflammation and tissue damage. In SLE, the presence of anti-dsDNA

, antibodies leads to chronic immune complex formation and widespread systemic

symptoms.


4. What is the primary cellular mediator responsible for the delayed-type hypersensitivity

(DTH) response observed in the Tuberculin skin test?

A. Mast cells


B. Th1 cells and Macrophages


C. B lymphocytes


D. Basophils


Answer: B


Rationale: DTH reactions are classified as Type IV hypersensitivity, which does not involve

antibodies but rather T cells. Upon secondary exposure to Mycobacterium tuberculosis

antigens, memory Th1 cells secrete IFN-gamma to activate macrophages. These activated

macrophages then cause the localized induration and inflammation seen 48 to 72 hours

after the test.


5. Which gene is essential for the expression of tissue-specific antigens in the thymus to

facilitate central tolerance?

A. STAT6


B. FoxP3


C. RAG1

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