What structure is recognized by TLR4 in mammals?

Correct Answer: B

Rationale: The correct answer is B: Lipopolysaccharide (LPS). TLR4 recognizes LPS, a component of the outer membrane of Gram-negative bacteria, triggering an immune response. This recognition is crucial in detecting bacterial infections. Peptidoglycan (A) is recognized by other TLRs, not TLR4. Double-stranded RNA (C) is recognized by TLR3, not TLR4. Mannose-binding lectin (D) is a pattern recognition receptor that binds to carbohydrate structures, not specifically recognized by TLR4.

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.

Correct Answer: B

Rationale: The correct answer is B: Alternative pathway. This pathway involves properdin, Factor B, and Factor D. Properdin stabilizes the C3 convertase complex formed by Factor B and Factor D, leading to the amplification of the complement cascade. The other choices are incorrect because: A: Classical pathway is initiated by antigen-antibody complexes binding to C1q. C: Lectin pathway is activated by lectins binding to carbohydrates on pathogen surfaces. D: Terminal pathway involves the formation of the membrane attack complex.

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.

Correct Answer: B

Rationale: The correct answer is B because clonal selection during lymphocyte activation leads to the formation of memory and effector cells. This process involves the proliferation and differentiation of the activated lymphocyte into these specialized cells, which play crucial roles in immune responses upon encountering the same antigen in the future. Cytokine suppression (choice A) is not the direct outcome of clonal selection but may be a regulatory mechanism during immune responses. Antigen elimination without cellular proliferation (choice C) is not accurate as clonal selection involves the expansion of specific lymphocyte clones. Destruction of the lymphocyte (choice D) is not the outcome of clonal selection, as activated lymphocytes undergo proliferation and differentiation rather than destruction.