Atherosclerosis is an autoimmune disease caused by self- and non-self-antigens contributing to excessive activation of T and B cell immune responses. These responses further aggravate vascular infiammation and promote progression of atherosclerosis and vulnerability to plaques via releasing pro-infiammatory cytokines. Regulatory T cells (Tregs) as the major immunoregulatory cells, in particular, induce and maintain immune homeostasis and tolerance by suppressing the immune responses of various cells such as T and B cells, natural killer (NK) cells, monocytes, and dendritic cells (DCs), as well as by secreting inhibitory cytokines interleukin (IL)-10, IL-35 and transcription growth factor β (TGF-β) in both physiological and pathological states. Numerous evidence demonstrates that reduced numbers and dysfunction of Treg may be involveved in atherosclerosis pathogenesis. Increasing or restoring the numbers and improving the immunosuppressive capacity of Tregs may serve as a fundamental immunotherapy to treat atherosclerotic cardiovascular diseases. In this article, we briefiy present current knowledge of Treg subsets, summarize the relationship between Tregs and atherosclerosis development, and discuss the possibilities of regulating Tregs for prevention of atherosclerosis pathogenesis and enhancement of plaque stability. Although the exact molecular mechanisms of Treg-mediated protection against atherosclerosis remain to be elucidated, the strategies for targeting the regulation of Tregs may provide specific and significant approaches for the prevention and treatment of atherosclerotic cardiovascular diseases.

中文翻译：

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调节性T细胞是动脉粥样硬化的新治疗靶标。

动脉粥样硬化是一种自身免疫和非自身抗原引起的自身免疫性疾病，导致T细胞和B细胞免疫反应的过度激活。这些反应通过释放促炎性细胞因子进一步加重了血管的炎症，并促进了动脉粥样硬化的发展和对斑块的易损性。调节性T细胞（Tregs）作为主要的免疫调节细胞，尤其是通过抑制T和B细胞，自然杀伤（NK）细胞，单核细胞和树突状细胞等各种细胞的免疫应答来诱导和维持免疫稳态和耐受性（ DCs），以及在生理和病理状态下都分泌抑制性细胞因子白介素（IL）-10，IL-35和转录生长因子β（TGF-β）。大量证据表明，Treg的数量减少和功能障碍可能与动脉粥样硬化的发病机理有关。增加或恢复Tregs的数量并提高其免疫抑制能力可作为治疗动脉粥样硬化性心血管疾病的基本免疫疗法。在本文中，我们简要介绍了当前Treg亚型的知识，总结了Treg与动脉粥样硬化发展之间的关系，并讨论了调节Treg预防动脉粥样硬化发病机理和增强斑块稳定性的可能性。尽管尚需阐明Treg介导的抗动脉粥样硬化保护作用的确切分子机制，