Regulatory T cells in ischemic stroke

Acta Pharmacol Sin. 2022 Jan;43(1):1-9. doi: 10.1038/s41401-021-00641-4. Epub 2021 Mar 26.

Abstract

Recent evidence shows that when ischemic stroke (IS) occurs, the BBB would be destructed, thereby promoting the immune cells to migrate into the brain, suggesting that the immune responses can play a vital role in the pathology of IS. As an essential subpopulation of immunosuppressive T cells, regulatory T (Treg) cells are involved in maintaining immune homeostasis and suppressing immune responses in the pathophysiological conditions of IS. During the past decades, the regulatory role of Treg cells has attracted the interest of numerous researchers. However, whether they are beneficial or detrimental to the outcomes of IS remains controversial. Moreover, Treg cells exert distinctive effects in the different stages of IS. Therefore, it is urgent to elucidate how Treg cells modulate the immune responses induced by IS. In this review, we describe how Treg cells fluctuate and play a role in the regulation of immune responses after IS in both experimental animals and humans, and summarize their biological functions and mechanisms in both CNS and periphery. We also discuss how Treg cells participate in poststroke inflammation and immunodepression and the potential of Treg cells as a novel therapeutic approach.

文章介绍: 免疫细胞浸润是调控卒中后神经损伤与修复的核心机制。调节性T (Treg) 细胞作为免疫抑制T细胞的重要亚群, 在缺血性脑卒中的病理进程中, 参与维持免疫稳态, 调控免疫反应等作用。既往研究表明, Treg细胞因缺血性脑卒中病理阶段不同而功能各异, 例如, Liesz等人证实, 脑卒中发生7天后, Treg细胞具有神经保护作用; 而Kleinschnitz等人发现, Treg 细胞缺失的DEREG小鼠在脑卒中1天后的梗死体积小于对照组, 证明Treg细胞在其中扮演有害角色。因此, 阐明Treg细胞如何调节缺血性脑卒中后免疫反应十分重要。在本篇综述中, 我们描述了Treg细胞在实验动物和人类发生缺血性脑卒中后的变化特征, 以及该细胞在调节免疫应答中的作用, 并讨论了Treg细胞如何参与缺血性脑卒中后炎症和免疫抑制的分子机制, 提出了Treg细胞作为一种新型细胞治疗方法的潜力及未来的研究方向。.

Keywords: crosstalk; inflammation; ischemic stroke; ischemic stroke therapy; regulatory T cells; stroke-induced immunodepression.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Ischemia / immunology*
  • Humans
  • Stroke / immunology*
  • T-Lymphocytes, Regulatory / immunology*