Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.2174/138920112798868700

Type

Journal article

Journal

Current pharmaceutical biotechnology

Publication Date

01/2012

Volume

13

Pages

77 - 87

Addresses

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

Keywords

Blood Vessels, Foam Cells, Animals, Humans, Ligands, Atherosclerosis, Toll-Like Receptors