Directing TRAF-ic: cell-specific TRAF6 signaling in chronic inflammation and atherosclerosis.

The recognition that atherosclerosis is a chronic inflammatory disease has emphasized the fundamental link between the innate immune system and disease pathogenesis. Atherosclerotic lesions develop at vulnerable locations throughout the vasculature as a result of detection of endogenous or microbial ligands by germ-line encoded pattern recognition receptors, including the innate immune Toll-like receptors (TLRs).1,2 Certain dietary lipids that contribute to atherosclerotic disease resemble on a molecular level lipids expressed in the microbial cell wall and are recognized by TLRs. Engagement via TLRs of dietary lipid molecules on both immune and nonimmune cells initiates inflammatory responses that persist chronically and culminate in the deposition of fatty streaks, which progress to occlusive atherosclerotic plaques.3