Purpose of review: Only recently has it been realized that immune mechanisms contribute to the pathophysiology of ischemic stroke, which for many years was regarded mainly as a vascular disease. These immunologic processes are present during all stages of stroke and involve both the innate and adaptive immune systems. This review highlights the latest findings related to the 'immunology of stroke'.
Recent findings: During the early phase of an ischemic insult, 'danger signals' such as ATP are released from dying tissue to subsequently attract inflammatory cells. Unexpectedly, T cells have been identified as prominent mediators of stroke-induced tissue damage. Whereas during the acute stage of infarction T cells act independently from antigen-specific stimuli but rather interact with thrombotic pathways, antigen-dependent T-cell activation might be relevant at later stages. Moreover, certain T-cell subsets like γδ T cells or regulatory T cells are able to influence stroke outcome either in a detrimental or beneficial way. Finally, proof-of-principle studies using FTY720 or VLA-4 blockers have demonstrated that the concept of 'immunomodulation in stroke' is feasible.
Summary: The insight that ischemic stroke at least in part is an immune-mediated disease may open new avenues for the treatment of this devastating neurologic condition.