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Originally published In Press as doi:10.1194/jlr.R800056-JLR200 on November 1, 2008

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Journal of Lipid Research, Vol. 50, S340-S345, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Atherogenesis

Emerging role of Toll-like receptors in atherosclerosis

Linda K. Curtiss1 and Peter S. Tobias

Department of Immunology and Microbial Science, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037

Published, JLR Papers in Press, November 1, 2008.

1 To whom correspondence should be addressed. email: lcurtiss{at}scripps.edu


ABSTRACT

Atherosclerosis is inflammation of the vessel wall of the arterial tree. This inflammation arises at specific areas that experience disturbed blood flow such as bifurcations and the lesser curvature of the aortic arch. Although all endothelial cells are exposed to comparable levels of circulating plasma cholesterol, only endothelial cells overlaying lesions display an inflamed phenotype. This occurs even in the absence of any additional exacerbating disease factors because blood flow controls the expression of Toll-like receptors (TLR), which are initiators of cellular activation and inflammation. TLR2- and 4-expression exert an overall proatherogenic effect in hyperlipidemic mice. TLR activation of the endothelium promotes lipid accumulation and leukocyte accumulation within lesions.

Supplementary key words endothelial cells • lipid accumulation • hypercholesterolemic mice • inflammation • leukocytes • bone marrow transplantation

Abbreviations: Hsp, heat shock protein; IL, interleukin; MyD88, myeloid differentiation factor 88; TLR, Toll-like receptors


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JLR 50th Anniversary Collections
Anniversary Collection::Atherogenesis

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