Abstract
See related article, p 1799. Changes in the adaptive immune system after focal cerebral ischemia are increasingly recognized to critically influence the outcome after stroke.1 In particular, T lymphocytes have been implicated as mediators of inflammatory brain tissue damage, but also as modulators of tissue remodeling. In addition, reductions in T-lymphocyte cellularity and function are prominent features of stroke-induced immunodepression and may increase the susceptibility to infection after stroke.2 T cells are, therefore, promising targets for developing novel stroke treatments. Recent experimental studies demonstrated that specific inhibition of T-cell trafficking into the ischemic brain by blockade of very late antigen-4 or vascular cell adhesion molecule-1 improved stroke outcome.3–5 These results in rodent stroke models led to the initiation of a phase II trial testing natalizumab in acute ischemic stroke, which is currently recruiting patients.6 In the present …
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