Nokea
Which rationale describes treatment of atopic allergies with immunotherapy?
- A. It decreases the levels of allergen-specific T helper cells.
- B. It decreases the level of IgE so that it does not react as readily with an allergen.
- C. It stimulates increased IgG to bind with allergen-reactive sites, preventing mast cell-bound IgE reactions.
- D. It gradually increases the amount of allergen in the body until it is no longer recognized as foreign and does not elicit an antibody reaction.
Correct Answer: C
Rationale: Immunotherapy stimulates the production of blocking IgG antibodies, which compete with IgE for allergen-binding sites, preventing mast cell activation.
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Which molecule released by NK cells is responsible for inducing apoptosis?
- A. Perforin
- B. Granzyme
- C. Cytokines
- D. Antibodies
Correct Answer: B
Rationale: The correct answer is B: Granzyme. Granzyme is the molecule released by NK cells that induces apoptosis in target cells. It enters the target cell through perforin, which creates pores in the target cell membrane. Cytokines are signaling molecules released by various immune cells but do not directly induce apoptosis. Antibodies are produced by B cells and do not induce apoptosis. Perforin aids in the delivery of granzyme but is not responsible for inducing apoptosis itself. Therefore, Granzyme is the correct choice for inducing apoptosis by NK cells.
What is the typical outcome of a C1q deficiency in the complement system?
- A. Enhanced inflammation
- B. Reduced phagocytosis
- C. Autoimmune diseases such as SLE
- D. Increased cancer risk
Correct Answer: C
Rationale: The correct answer is C: Autoimmune diseases such as SLE. C1q is essential for the classical pathway of the complement system, which plays a crucial role in clearing immune complexes. A deficiency in C1q can lead to impaired immune complex clearance, resulting in the development of autoimmune diseases like Systemic Lupus Erythematosus (SLE).
Choice A (Enhanced inflammation) is incorrect because a deficiency in C1q would actually lead to decreased inflammation due to impaired complement activation.
Choice B (Reduced phagocytosis) is incorrect because phagocytosis is primarily mediated by the alternative pathway of the complement system, not the classical pathway involving C1q.
Choice D (Increased cancer risk) is incorrect as C1q deficiency is not directly associated with an increased risk of cancer.
Which of the following is considered a defining characteristic of a TH2 response?
- A. Production of IgM antibodies
- B. Activation of CTL
- C. Recruitment and activation of neutrophils
- D. Production of IgE antibodies
Correct Answer: D
Rationale: The correct answer is D: Production of IgE antibodies. A TH2 response is characterized by the production of IgE antibodies, which are essential in allergic reactions. IgM antibodies (A) are produced during the primary immune response. Activation of CTL (B) is associated with a TH1 response. Neutrophils (C) are primarily involved in the innate immune response and are not specific to TH2 responses. In summary, the production of IgE antibodies is a defining characteristic of a TH2 response, distinguishing it from other immune responses.
A cytokine polarizing activated T cells towards a TH2 subset is
- A. IL-12
- B. IL-2
- C. IL-10
- D. IL-5
Correct Answer: C
Rationale: The correct answer is C: IL-10. IL-10 is known to polarize activated T cells towards a TH2 subset by suppressing TH1 cytokine production. IL-12 (A) promotes TH1 differentiation, IL-2 (B) supports T cell proliferation, and IL-5 (D) is involved in eosinophil activation and differentiation, not in polarizing T cells towards a TH2 subset.
Drugs aimed at blocking the budding of HIV from the host cell
- A. Are RT inhibitors
- B. Should target gp120
- C. Should target HIV co-receptors
- D. Are protease inhibitors
Correct Answer: D
Rationale: The correct answer is D: Are protease inhibitors. Blocking HIV budding involves inhibiting the action of the viral protease enzyme, which is crucial for processing viral proteins into their functional forms. By targeting protease, the virus cannot mature and infect new cells. RT inhibitors (A) target reverse transcriptase, not budding. Targeting gp120 (B) is focused on viral entry, not budding. Targeting HIV co-receptors (C) is aimed at blocking viral entry, not budding.