Ley Klaus, Gerdes Norbert, Winkels Holger
From the Division of Inflammation Biology, La Jolla Institute for Allergy & Immunology, CA (K.L., H.W.); Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Hospital Düsseldorf, Germany (N.G.); and Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.).
Arterioscler Thromb Vasc Biol. 2017 May;37(5):764-777. doi: 10.1161/ATVBAHA.117.308611. Epub 2017 Mar 30.
Immune cells play a critical role in atherosclerosis. Costimulatory and coinhibitory molecules of the tumor necrosis factor receptor and CD28 immunoglobulin superfamilies not only shape T-cell and B-cell responses but also have a major effect on antigen-presenting cells and nonimmune cells.
Pharmacological inhibition or activation of costimulatory and coinhibitory molecules and genetic deletion demonstrated their involvement in atherosclerosis. This review highlights recent advances in understanding how costimulatory and coinhibitory pathways shape the immune response in atherosclerosis.
Insights gained from costimulatory and coinhibitory molecule function in atherosclerosis may inform future therapeutic approaches.
免疫细胞在动脉粥样硬化中起关键作用。肿瘤坏死因子受体和CD28免疫球蛋白超家族的共刺激和共抑制分子不仅塑造T细胞和B细胞反应,而且对抗抗原呈递细胞和非免疫细胞有重大影响。
共刺激和共抑制分子的药理学抑制或激活以及基因缺失证明了它们参与动脉粥样硬化。本综述重点介绍了在理解共刺激和共抑制途径如何塑造动脉粥样硬化中的免疫反应方面的最新进展。
从动脉粥样硬化中共刺激和共抑制分子功能获得的见解可能为未来的治疗方法提供信息。