Yanbao Xiong

TL;DR: The D299G polymorphism compromises recruitment of MyD88 and TRIF toTLR4 without affecting TLR4 expression, TLR 4–MD2 interaction, or LPS binding, suggesting that it interferes with TLR3 dimerization and assembly of intracellular docking platforms for adapter recruitment.

TL;DR: Induction of endotoxin tolerance in vivo inhibits expression of proinflammatory mediators via impaired activation of IRAK4, p38, and NF‐κB and increases expression of negative regulators of TLR4 pathways.

TL;DR: Deficiencies in these signaling events in LPS-tolerant cells coincided with increased expression of A20, an essential deubiquitination enzyme, and sustained A20-IRAK1 associations, which are new determinants of endotoxin tolerance.

TL;DR: The R753Q polymorphism renders TLR2 signaling-incompetent by impairing its tyrosine phosphorylation, dimerization with TLR6, and recruitment of Mal and MyD88, and facilitates design of new therapeutic strategies.

TL;DR: Different roles for S1PRs are demonstrated in comodulating T cell and LEC functions in migration and suggest previously unknown levels of regulation of leukocytes and endothelial cells during homeostasis and immunity.