Stroke-induced immunosuppression and T helper cells 17 / 中国脑血管病杂志

ABSTRACT

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 Thl7 cells.