Fig. 2

Functions of T cell subsets in the acute and chronic phases after ischaemic stroke. In the acute phase, necrotic cells release DAMPs to activate brain-resident microglia, and then activated microglia secrete cytokines, such as IL-23, to recruit γδ T cells via an antigen-independent pathway. IL-17 released by γδ T cells, other inflammatory cytokines and antigens from the injured brain induce antigen-dependent immune responses by Th1, Th2, Th17 and Th40 cells. Th2 cells exert a protective role by promoting microglial M2 polarization. Other cells interact with M1 microglia to play detrimental roles in the injured brain or secrete proinflammatory cytokines. In the chronic phase, Treg cells may exist until 1 month after stroke onset and perform roles in recovery via several pathways, including scar formation, neuronal repair and revascularization