Stroke results in cerebral inflammation that causes brain injury and triggers immunodepression, resulting in an increased incidence of morbidity and mortality secondary to remote infection. It is well known that T cells modulate brain inflammation after ischemic stroke, and targeting T cells may be an innovative therapeutic strategy for stroke treatment. T cell deficiency is neuro-protective, but the observed protective effects differ between ischemic models. Recent studies suggest different T cell subsets may have distinct effects on the injured brain. In addition to their role in cerebral inflammation, T cells also play a role in stroke-induced immunodepression. Therefore, T cell-targeted therapies designed to provide protection against brain inflammation might paradoxically contribute to remote organ infection and mortality. Further investigations are required to determine the role of specific T cell subsets in cerebral inflammation and stroke-induced immunodepression, the optimal therapeutic window for treatment, and the appropriate dose of anti-T cell therapy.