Tobias Peter, Curtiss Linda K
Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
J Lipid Res. 2005 Mar;46(3):404-11. doi: 10.1194/jlr.R400015-JLR200. Epub 2005 Jan 16.
Atherosclerosis is a chronic inflammatory response characterized by the accumulation of cells of innate and acquired immune systems within the intima of the arterial wall. Macrophages are the predominant participant in innate immune responses in atherosclerosis. Protein receptors expressed by macrophages and endothelial cells recognize components and products of microorganisms and play a vital role in innate immunity. In particular, the members of the toll-like receptor (TLR) family play a critical role in the inflammatory components of atherosclerosis. Both exogenous ligands involved in microbial recognition as well as endogenous ligands involved in sterile inflammation pathways are implicated in the pathology of atherosclerosis. In this review, we discuss our current understanding of the role of TLRs and their coactivators in atherosclerosis, with particular emphasis on studies in atherosclerosis-prone hypercholesterolemic mice.
动脉粥样硬化是一种慢性炎症反应,其特征是先天性和获得性免疫系统的细胞在动脉壁内膜积聚。巨噬细胞是动脉粥样硬化先天性免疫反应的主要参与者。巨噬细胞和内皮细胞表达的蛋白质受体识别微生物的成分和产物,并在先天性免疫中起关键作用。特别是,Toll样受体(TLR)家族成员在动脉粥样硬化的炎症成分中起关键作用。参与微生物识别的外源性配体以及参与无菌炎症途径的内源性配体都与动脉粥样硬化的病理过程有关。在这篇综述中,我们讨论了目前对TLR及其共激活因子在动脉粥样硬化中作用的理解,特别强调了对易患动脉粥样硬化的高胆固醇血症小鼠的研究。