Yersinia pestis, the causative agent of the bubonic plague, has multiple mechanisms of immune evasion. This Gram-negative bacterium is transmitted from fleas (body temperature, 26°C) to humans (body temperature, 37°C) by flea bites. Studies have shown that the lipopolysaccharide (LPS) produced by Y. pestis grown at 37°C is about 10-fold less potent at stimulating TLR4 signaling than is the Y. pestis LPS from bacteria grown at 26°C. When these two forms of Y. pestis LPS are compared for their abilities to induce responses from human macrophages, one would expect that the 26°C Y. pestis LPS would result in:
A) Increased production of antimicrobial peptides
B) Reduced production of IL-10
C) Increased production of TNF- and IL-6
D) Reduced production of Type I interferons
E) Increased activation of the inflammasome
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