Yasuharu Watanabe

TL;DR: It is shown that ILG potently inhibits the activation of NLRP3 inflammasome, and the effect is independent of its inhibitory potency on TLR4.

TL;DR: The in vitro study revealed that lipopolysaccharide-treated bone marrow–derived macrophages directly inhibited the expression of angiogenic factors in 3T3-L1 preadipocytes, indicating that macrophage HIF-1α is involved not only in the formation of CLSs, further enhancing the inflammatory responses, but also in the inhibition of neoangiogenesis in preadIPocytes.

TL;DR: It is shown that ILG suppresses adipose tissue inflammation by affecting the paracrine loop containing saturated fatty acids and TNF-α by using a co-culture composed of adipocytes and macrophages and ILG suppressed inflammatory changes induced by the co- culture through inhibition of NF-κB activation.

TL;DR: How various pattern recognition receptors in the immune system underlie the etiology of obesity-associated inflammation and insulin resistance is discussed, with a particular focus on the TLR (Toll-like receptor) family protein Radioprotective 105 (RP105)/myeloid differentiation protein-1 (MD-1).

TL;DR: The RP105/MD-1 complex is a major mediator of adipose tissue inflammation independent of TLR4 signaling and may represent a novel therapeutic target for obesity-associated metabolic disorders.