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This process entails the adhesion of the peripheral immune cells to endothelial cells, which facilitates their translocation across the blood-brain barrier, ultimately resulting in barrier disruption, cerebral edema, and brain injury, which indirectly promote the infiltration of peripheral immune cells ( + cytotoxic T cells are the first T cell subset to infiltrate the infarct lesion within hours after stroke, whereas CD4 + and natural killer T cells appear at approximately 24 hours after the onset of ischemia ( + T cells significantly increased in the ipsilateral brain, not only in the distal core but also in the corpus callosum ( Table 2 The infiltrating situation of different subtypes of immune cells after the onset of ischemic stroke