Zhuang Rulin, Feinberg Mark W
Department of Medicine, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA; Department of Cardiovascular Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
Department of Medicine, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
J Mol Cell Cardiol. 2020 Oct;147:1-11. doi: 10.1016/j.yjmcc.2020.08.004. Epub 2020 Aug 7.
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.
缺血性损伤引发增强的炎症反应,这对组织修复至关重要,但过度和慢性的炎症反应会促进缺血性心血管疾病的发病机制。调节性T细胞(Tregs)是自身耐受性和免疫抑制的主要调节因子,可控制先天性和适应性免疫反应,调节特定免疫细胞亚群,防止过度炎症,并参与缺血后的组织修复。在此,我们总结了Tregs发挥抑制功能的多种潜在机制,包括细胞因子产生的调节、细胞间相互作用的改变以及代谢途径的破坏。此外,我们回顾了Tregs在缺血性损伤和修复中的作用,包括心肌、肢体和脑缺血。我们最后展望了Treg生物学在理解缺血性心血管疾病发病机制方面的治疗机会和未来挑战。