Nokea
Which compounds produced by microorganisms can cause fever in humans and can withstand autoclaving?
- A. endotoxin
- B. Lipid A
- C. lipopolysaccharide
- D. peptidoglycan
Correct Answer: D
Rationale: The correct answer is D, peptidoglycan. Peptidoglycan is a component of bacterial cell walls that can trigger fever in humans. It is a sturdy molecule that can withstand autoclaving.
A: Endotoxin is a component of the outer membrane of Gram-negative bacteria, not resistant to autoclaving.
B: Lipid A is the toxic component of endotoxin, not resistant to autoclaving.
C: Lipopolysaccharide is the major component of the outer membrane of Gram-negative bacteria, not resistant to autoclaving.
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The 'major histocompatibility complex' (MHC) proteins involved in antigen presentation to T cells were first noted during studies of:
- A. Innate immunity
- B. Allergy
- C. Transplantation
- D. Autoimmunity
Correct Answer: C
Rationale: The correct answer is C: Transplantation. MHC proteins play a crucial role in transplant rejection by presenting antigens to T cells, initiating an immune response against foreign tissues. This discovery was significant in understanding transplant immunology. Choices A, B, and D are incorrect because innate immunity involves nonspecific defense mechanisms, allergies are mediated by IgE antibodies, and autoimmunity involves the immune system attacking self-antigens, none of which directly relate to the discovery of MHC proteins in transplantation studies.
TLR-3 detects viruses found in:
- A. Cytosol
- B. Extracellular space
- C. Endosomes
- D. All of the above
Correct Answer: C
Rationale: TLR-3 detects viruses in endosomes. When a virus enters a host cell, it is often engulfed into endosomes. TLR-3 recognizes viral RNA within endosomes and triggers an immune response. Choices A and B are incorrect because TLR-3 does not detect viruses in the cytosol or extracellular space. Choice D is incorrect because TLR-3 specifically functions in endosomes to detect viral RNA.
What drives the emergence of immuno-resistant pathogen strains?
- A. Host immune system failure
- B. Slow mutation rates in pathogens
- C. Rapid pathogen reproduction and mutations
- D. Absence of host immune adaptation
Correct Answer: C
Rationale: The correct answer is C: Rapid pathogen reproduction and mutations drive the emergence of immuno-resistant pathogen strains. This is because the high rate of reproduction allows for more opportunities for mutations to occur, some of which may confer resistance to the host's immune system or medical interventions. Slow mutation rates in pathogens (B) would not lead to the rapid emergence of resistant strains. Host immune system failure (A) occurs after the pathogen has already developed resistance. The absence of host immune adaptation (D) does not directly drive the emergence of resistant strains as it is the rapid reproduction and mutations of pathogens that play a crucial role.
When was the first vaccine for smallpox developed?
- A. 1726
- B. 1796
- C. 1882
- D. 1895
Correct Answer: B
Rationale: The correct answer is B: 1796. This is because the first vaccine for smallpox was developed by Edward Jenner in 1796. He used cowpox virus to create immunity against smallpox. Choices A, C, and D are incorrect because they do not align with historical records of the development of the smallpox vaccine. Choice A (1726) is too early, choices C (1882) and D (1895) are much later dates and do not correspond to the actual timeline of the smallpox vaccine's discovery.
What is the primary role of Helper T cells in the immune response?
- A. Killing infected host cells
- B. Producing antibodies
- C. Secreting cytokines to activate other immune cells
- D. Suppressing immune responses
Correct Answer: C
Rationale: Helper T cells primarily secrete cytokines to activate other immune cells. This is crucial for coordinating and amplifying the immune response. They do not kill infected host cells (A), as that is the role of cytotoxic T cells. Producing antibodies (B) is the function of B cells. Suppressing immune responses (D) is the role of regulatory T cells, not Helper T cells.