{"title":"The Sunlight: A New Immunomodulatory Approach of Atherosclerosis.","authors":"H. Ait-Oufella, A. Sage","doi":"10.1161/ATVBAHA.116.308637","DOIUrl":null,"url":null,"abstract":"Atherosclerosis is a pathological condition of the arterial wall that underlies adverse vascular events, including myocardial infarction, stroke, and ischemic gangrene, and is responsible for most of the cardiovascular morbidity and mortality in the Western world. The past 2 decades have witnessed major advances in our understanding of the pathophysiology of atherosclerosis especially the identification of a central role for innate and adaptive immune responses in arterial disease development and potentially disease complications.1 Among CD4+ T lymphocytes, interferon (IFN)-γ-producing T helper type 1 cells have been shown to exert proatherogenic effects, whereas regulatory T cells (Tregs) display atheroprotective properties.2 Tregs act through several pathways, including provision of interleukin (IL)-10 or transforming growth factor (TGF)-β, control of IL-2 availability, or cell–cell contact-dependent inhibitory mechanisms, for example, CTLA-4 expression and transendocytosis of costimulatory molecules.3,4 The identification of a critical protective role of Tregs in atherosclerosis5 has led to studies aimed at promoting Treg responses in vivo to tame disease development. Both antigen-specific and nonspecific strategies have been tested successfully in mouse models of atherosclerosis. Among the antigen-nonspecific approaches, treatment with selective anti-CD3 antibodies6 or treatment with IL-2,7 which substantially increased endogenous Tregs levels and halted disease …","PeriodicalId":8404,"journal":{"name":"Arteriosclerosis, Thrombosis, & Vascular Biology","volume":"34 1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Arteriosclerosis, Thrombosis, & Vascular Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1161/ATVBAHA.116.308637","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Atherosclerosis is a pathological condition of the arterial wall that underlies adverse vascular events, including myocardial infarction, stroke, and ischemic gangrene, and is responsible for most of the cardiovascular morbidity and mortality in the Western world. The past 2 decades have witnessed major advances in our understanding of the pathophysiology of atherosclerosis especially the identification of a central role for innate and adaptive immune responses in arterial disease development and potentially disease complications.1 Among CD4+ T lymphocytes, interferon (IFN)-γ-producing T helper type 1 cells have been shown to exert proatherogenic effects, whereas regulatory T cells (Tregs) display atheroprotective properties.2 Tregs act through several pathways, including provision of interleukin (IL)-10 or transforming growth factor (TGF)-β, control of IL-2 availability, or cell–cell contact-dependent inhibitory mechanisms, for example, CTLA-4 expression and transendocytosis of costimulatory molecules.3,4 The identification of a critical protective role of Tregs in atherosclerosis5 has led to studies aimed at promoting Treg responses in vivo to tame disease development. Both antigen-specific and nonspecific strategies have been tested successfully in mouse models of atherosclerosis. Among the antigen-nonspecific approaches, treatment with selective anti-CD3 antibodies6 or treatment with IL-2,7 which substantially increased endogenous Tregs levels and halted disease …