Pastrana Jahaira Lopez, Sha Xiaojin, Virtue Anthony, Mai Jietang, Cueto Ramon, Lee In Ae, Wang Hong, Yang Xiao-Feng
Cardiovascular Research Center, Department of Pharmacology and Thrombosis Research Center, Temple University School of Medicine, Philadelphia, PA 19140.
J Clin Exp Cardiolog. 2012 Oct 8;2012(Suppl 12):2. doi: 10.4172/2155-9880.S12-002.
Atherosclerosis is a chronic autoimmune inflammatory disease. The involvement of both innate and adaptive immune responses in the pathogenesis of the disease has been well recognized. Tregs are an essential part of the immune system and have indispensable functions in maintaining immune system homeostasis, mediating peripheral tolerance, preventing autoimmune diseases, and suppressing inflammatory and proatherogenic immune response. Tregs carry out their immunosuppressive functions via several mechansims. One of the well-documented suppressive mechanisms of Tregs is the secretion of anti-inflammatory cytokines including IL-10, TGF-β, and IL-35. Studies have found that IL-10 and TGF-β have atheroprotective properties. In addition, Tregs can suppress the activity of proatherogenic effector T cells, suggesting an atheroprotective role. In fact, fewer Tregs are found in atherogenic -/- mice comparing to wild-type mice, suggesting an uncontrolled balance between weakened Tregs and effector T cells in atherogenesis. Some clinical studies of autoimmune diseases also suggest that decreased Tregs numbers are associated with increased disease activity. The importance of Tregs in many autoimmune diseases and experimental atherosclerosis has been established in and studies. However, the roles of Tregs in atherosclerosis in the clinical setting remains to be further characterized.
动脉粥样硬化是一种慢性自身免疫性炎症性疾病。固有免疫反应和适应性免疫反应在该疾病发病机制中的参与已得到充分认识。调节性T细胞（Tregs）是免疫系统的重要组成部分，在维持免疫系统稳态、介导外周耐受、预防自身免疫性疾病以及抑制炎症和促动脉粥样硬化免疫反应方面具有不可或缺的作用。Tregs通过多种机制发挥其免疫抑制功能。Tregs有充分文献记载的抑制机制之一是分泌抗炎细胞因子，包括白细胞介素-10（IL-10）、转化生长因子-β（TGF-β）和白细胞介素-35（IL-35）。研究发现，IL-10和TGF-β具有抗动脉粥样硬化特性。此外，Tregs可抑制促动脉粥样硬化效应T细胞的活性，提示其具有抗动脉粥样硬化作用。事实上，与野生型小鼠相比，在动脉粥样硬化模型的基因敲除小鼠中发现的Tregs较少，这表明在动脉粥样硬化过程中，Tregs减弱与效应T细胞之间的平衡失控。一些自身免疫性疾病的临床研究也表明，Tregs数量减少与疾病活动增加有关。Tregs在许多自身免疫性疾病和实验性动脉粥样硬化中的重要性已在相关研究中得到证实。然而，Tregs在临床环境中动脉粥样硬化中的作用仍有待进一步明确。
