Abstract
Abstract Dysregulation in Toll-like receptor (TLR) signaling has been implicated in many disease states, including chronic inflammatory conditions such as atherosclerosis. The cytoplasmic adaptor proteins TNF receptor associated factor (TRAF)3 and TRAF6 are known to mediate TLR signaling. Recent data from our lab demonstrate for the first time that TRAF5 also plays a significant role in immune cell TLR functions. B lymphocytes, macrophages, and dendritic cells from TRAF5-/- mice show increased cytokine production and enhanced early signaling pathways after stimulation through various TLRs. Interestingly, B cell TLR responses are the most greatly affected by TRAF5 deficiency. Our data show that TRAF5 is a negative regulator of TLR signaling and restrains proinflammatory cytokine production. It has been reported that TRAF5 deficiency accelerates the development of atherosclerosis in mice, while human patients with coronary heart disease express lower levels of TRAF5 mRNA in blood compared with healthy controls. Elucidating the role of TRAF5 in TLR signaling may provide a new target for therapies against a variety of inflammatory conditions, including those predisposing to atherogenesis. Our current studies focus on identifying the key molecular interactions by which TRAF5 mediates its effects on TLR pathways.
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