FasL incapacitation alleviates CD4+ T cells-induced brain injury through remodeling of microglia polarization in mouse ischemic stroke.

Inflammation responses involving the crosstalk between infiltrated T cells and microglia play crucial roles in ischemia stroke. Recent studies showed that Fas ligand (FasL) mutation could reduce post-stroke T cell invasion and microglia activation. In this study, we demonstrated that CD4+ T cells could induce M1 microglia polarization through NF-κB signaling pathway, whereas FasL mutant CD4+ T cells significantly reversed this effect. Besides, Th17/Treg cells balance was skewed into Treg cells after FasL mutation. In addition, conditioned medium from co-culture of FasL mutant CD4+ T cells and microglia could alleviate neuronal injury. Collectively, FasL incapacitation could alleviate CD4+ T cells-induced inflammation through remodeling microglia polarization, suggesting a therapeutic potential for control of inflammation responses after ischemic stroke.