卒中后免疫抑制与辅助性T细胞17变化的研究进展

Stroke-induced immunosuppression and T helper cells 17

卒中急性期,损伤脑组织释放炎性介质触发炎性级联反应,进一步加重脑损伤,随后卒中可诱导免疫抑制以减轻炎性反应并发挥脑保护的作用。辅助性T细胞(Th) 17及其主要效应因子白细胞介素17A在卒中后增加,进一步促进卒中后炎性反应,加重神经功能缺损。而卒中后免疫抑制相关通路可对Th细胞亚群进行调节,反馈作用于Th17细胞。

In the acute phase of stroke,the injured brain tissue releases inflammatory mediators to trigger the inflammatory cascade reaction.As a result,the Interleukin 17A,a major effector of T helper(Th)cells 17,increases after stroke,further contribute to the inflammatory response and aggravated the neurological deficits.Then the stroke induces immune suppression to suppress the inflammatory response,thus play a role in brain protection.The relevant pathways of post-stroke immunosuppression can regulate the Th cell subset and exert feedback effects on Th17 cells.