Th17 Cells and IL-17A in Ischemic Stroke

Abstract

The neurological injury and repair mechanisms after ischemic stroke are complex. The inflammatory response is present throughout stroke onset and functional recovery, in which CD4 + T helper(Th) cells play a non-negligible role. Th17 cells, differentiated from CD4 + Th cells, are regulated by various extracellular signals, transcription factors, RNA, and post-translational modifications. Th17 cells specifically produce interleukin-17A(IL-17A), which has been reported to have pro-inflammatory effects in many studies. Recently, experimental researches showed that Th17 cells and IL-17A play an important role in promoting stroke pathogenesis (atherosclerosis), inducing secondary damage after stroke, and regulating post-stroke repair. This makes Th17 and IL-17A a possible target for the treatment of stroke. In this paper, we review the mechanism of action of Th17 cells and IL-17A in ischemic stroke and the progress of research on targeted therapy.

Network-pharmacology-based study on the mechanism of fibrates regulating HIF-1A in the treatment of ischemic stroke

“…KEGG pathway enrichment analysis showed that brates can regulate HIF1A to prevent and treat IS through Th17 cell differentiation, thyroid hormone signaling pathway and HIF-1 signaling pathway. The pathway of Th17 cells differentiation is related to a variety of in ammatory factors such as TGF-β, IL-17A, IL-6, IL-21 and IL-22, which are involved in the occurrence and progression of many in ammatory reactions and autoimmune diseases 39 . Fibrates may reduce the occurrence of vascular in ammation reactions by inhibiting in ammatory factors, which can reduce the level of HIF1A factor, it can increase cerebral blood perfusion and reduce the occurrence of cerebral hypoxia and ischemia symptoms.…”

Pathogenic role of different phenotypes of immune cells in airway allergic diseases: a study based on Mendelian randomization

“…In addition to Th1/Th2 imbalance, Treg/Th17 is an important influence on the pathogenesis of airway allergic inflammation ( 21 , 22 ); there is a very complex link between Th17 and Treg, which both diverge from naïve CD4+ T cells, which can differentiate into Treg only when induced by TGF-β. When TGF-β and IL-6 are present at the same time, the CD4 + T cells will turn to differentiate into Th17, this process is in a state of dynamic equilibrium, which maintains a stable immune state of the organism, when there is an imbalance of the cytokine environment in the surroundings, the production of Treg decreases, and the production of Th17 increases, which aggravate the allergic inflammation and the high reaction of the airways ( 23 , 24 ). In conclusion, classical Treg is important for keeping immune stability and suppressing the onset of autoimmune diseases.…”