Fig. 3

Different T cell subsets infiltrate the injured brain. Th1 cells secrete proinflammatory cytokines, such as IFN-γ and TNF-α, to promote M1 polarization. M1 microglia also induce and recruit Th1 cells by secreting IL-12 and TNF-α and expressing chemokines, such as CXCL9 and CXCL10. Moreover, Th2 cells secrete anti-inflammatory cytokines, such as IL-4, IL-10 and IL-13, to promote M2 polarization, and M2 cells can induce and recruit Th2 cells by secreting IL-4, CCL17, CCL22 and CCL24. Th40 cells, which are proinflammatory, secrete both IFN-γ and IL-17A and infiltrate the injured brain in the early stage after brain injury. γδ T cells secrete proinflammatory IL-17 to aggravate brain injury. Moreover, γδ T cells and Th17 cells activate proinflammatory microglia by modulating the FasL/PTPN2/TNF-α signalling pathway, which aggravates ischaemic brain injury. Treg cells interact with microglia and modulate microglial polarization from the M1 phenotype into the M2 phenotype via IL-10, and they also regulate astrogliosis by producing the cytokine amphiregulin (Areg). CD8⁺ T cells can recruit CD4⁺ mononuclear cells via the cytokine IL-16 after femoral artery ligation, and CD4⁺ T cells contribute to the imbalance in M1 and M2 polarization