title: The tolls and dangers of atherosclerotic disease.
abstract: 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.
authors.affiliation: Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, University of Oxford, 65 Aspenlea Road, London W6 8LH, United Kingdom. claudia.monaco@kennedy.ox.ac.uk
authors.forename: Claudia
authors.initials: C
authors.lastname: Monaco
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000276:immunology*; D001808:Blood Vessels / Q000276:immunology; D005487:Foam Cells / Q000276:immunology; D006801:Humans; D008024:Ligands; D051193:Toll-Like Receptors / Q000819:agonists / Q000276:immunology*
chemical_list: D008024:Ligands; D051193:Toll-Like Receptors