Dynamics of T cell responses after stroke

• T cells serve both inflammatory and protective roles in acute stroke.
• Effects are direct and through modulation of the inflammatory milieu.
• Following the early phase, there is a shift towards repair.
• In the late phase, T cells may cause chronic inflammation.
• There may be potential for therapeutic agents to limit immune-mediated injury.

T cells are integral to the pathophysiology of stroke. The initial inflammatory cascade leads to T cell migration, which results in deleterious and protective effects mediated through CD4(+), CD(8)+, γδ T cells and regulatory T cells, respectively. Cytokines are central to the T cell responses, with key roles established for TNF-α, IFN-γ, IL-17, IL-21 and IL-10. Through communication with the systemic immune system via neural and hormonal pathways, there is also transient immunosuppression after severe strokes. With time, the inflammatory process eventually transforms to one more conducive of repair and recovery, though some evidence also suggests ongoing chronic inflammation. The role of antigen-specific T cell responses requires further investigation. As our understanding develops, there is increasing scope to modulate the T cell response after stroke.