ABSTRACT
Atherosclerosis is a chronic inammatory disease where both innate and adaptive immune responses are intimately involved in its pathogenesis. Oxidation-specic epitopes (OSE) represent danger-associated molecular patterns (DAMPs) that promote inammation and cell death. Oxidized phospholipids (OxPL) are well-studied OSE generated during oxidation of low-density lipoprotein (OxLDL) and of cells undergoing apoptosis. OxPL are highly immunogenic, pro-inammatory and are present in atherosclerotic lesions of animals and humans, particularly in pathologically dened vulnerable and disrupted plaques. OxPL are important contributors to early and late events in atherogenesis by activating pro-inammatory genes, leading to inammatory cascades in the vessel wall. The interaction of lipid accumulation, generation of OxPL, activation of inammatory processes, recruitment of inammatory cells, endothelial dysfunction, platelet activation, and thrombosis ultimately leads to plaque progression and clinical events. Innate and adaptive immune mechanisms play a central role throughout these events, resulting in atherosclerotic lesions having many features of a chronic inammatory disease. Over the last decade, it has been demonstrated by a variety of studies that OxPL are carried by lipoprotein (a)
Introduction ............................................................................................................ 281 OxPL and Innate and Adaptive Immunity ............................................................. 282 Effects of OxPL on Cells Associated with Atherosclerosis ...................................284
