Inflammation drives atherosclerosis. Toll-like receptor-2 and -4 are so far the strongest candidates for initiating innate immune signalling in atherosclerosis. Their signalling has implications for lesion development, foam cell formation, inflammation, matrix degradation and ischemia-reperfusion. The repertoire of TLR agonists is expanding. They collectively represent a conglomerate of structurally diverse molecular patterns requiring a high level of versatility in their sensing. Such versatility is achieved through cooperation of TLR heterodimers, co-receptors, and binding proteins. Several endogenous and exogenous molecular patterns engaging TLRs are associated with atherosclerosis development and complications. In this review, I describe how such molecular patterns are sensed, how they signal and what the consequences in the atherosclerotic plaque might be. The effect of TLR antagonising compounds in human and murine atherosclerosis is also addressed.
Keywords: Atherosclerosis, inflammation, innate immunity, toll-like receptors, Toll-like receptor-2 and -4, lesion development, foam cell formation, matrix degradation and, ischemia-reperfusion, TLR heterodimers, TLRs, blood-borne inflammatory cells, humoral immune responses, inflammatory arthritis, Tolllike-receptors (TLRs)
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