The Sunlight: A New Immunomodulatory Approach of Atherosclerosis.

H. Ait-Oufella, A. Sage
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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 …
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阳光:一种新的动脉粥样硬化免疫调节途径。
动脉粥样硬化是动脉壁的一种病理状态,是不良血管事件的基础,包括心肌梗死、中风和缺血性坏疽,是西方世界大多数心血管发病率和死亡率的原因。在过去的20年里,我们对动脉粥样硬化病理生理学的理解取得了重大进展,特别是在动脉疾病发展和潜在疾病并发症中先天性和适应性免疫反应的核心作用的确定在CD4+ T淋巴细胞中,干扰素(IFN)-γ产生T辅助型1细胞已被证明具有促动脉粥样硬化作用,而调节性T细胞(Tregs)则显示出动脉粥样硬化保护特性Tregs通过多种途径发挥作用,包括提供白细胞介素(IL)-10或转化生长因子(TGF)-β,控制IL-2的可用性,或细胞-细胞接触依赖的抑制机制,例如CTLA-4的表达和共刺激分子的转内吞作用。3,4 Treg在动脉粥样硬化中的关键保护作用的确定,导致了旨在促进体内Treg反应以抑制疾病发展的研究。抗原特异性和非特异性策略已经在动脉粥样硬化小鼠模型中成功地进行了测试。在抗原非特异性方法中,使用选择性抗cd3抗体治疗6或使用il -2,7治疗可显著增加内源性Tregs水平并阻止疾病发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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Editors and Editorial Board. Correction to: Role of LpL (Lipoprotein Lipase) in Macrophage Polarization In Vitro and In Vivo. Tribute to Paul M. Vanhoutte, MD, PhD (1940-2019). Correction to: 18F-Sodium Fluoride Imaging of Coronary Atherosclerosis in Ambulatory Patients With Diabetes Mellitus. Extracellular MicroRNA-92a Mediates Endothelial Cell-Macrophage Communication.
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