Ischemic injury triggers a heightened inflammatory response that is essential for tissue repair, but excessive and chronic inflammatory responses contribute to the pathogenesis of ischemic cardiovascular disease. Regulatory T cells (Tregs), a major regulator of self-tolerance and immune suppression, control innate and adaptive immune responses, modulate specific immune cell subsets, prevent excessive inflammation, and participate in tissue repair after ischemia. Herein, we summarize the multiple potential mechanisms by which Tregs exert suppressor functions including modulation of cytokine production, alteration of cell-cell interactions, and disruption of metabolic pathways. Furthermore, we review the role of Tregs implicated in ischemic injury and repair including myocardial, limb, and cerebral ischemia. We conclude with a perspective on the therapeutic opportunities and future challenges of Treg biology in understanding the pathogenesis of ischemic cardiovascular disease states.

缺血性损伤触发了对于组织修复必不可少的炎症反应，但过度和慢性炎症反应会导致缺血性心血管疾病的发病机理。调节性T细胞（Tregs）是自我耐受和免疫抑制的主要调节剂，可控制先天性和适应性免疫反应，调节特定的免疫细胞亚群，防止过度炎症，并参与缺血后的组织修复。本文中，我们总结了Treg发挥抑制功能的多种潜在机制，包括调节细胞因子的产生，改变细胞与细胞的相互作用以及破坏代谢途径。此外，我们审查了涉及缺血性损伤和修复（包括心肌，肢体和脑缺血）的Treg的作用。