ICAM-1 as a Potential Target for Treatments Blocking the Host Response in Stroke.

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Abstract

Leukocytes and their actions have been implicated in the pathogenesis of microcirculatory and cytotoxic perturbations in experimental stroke models. Experiments in several models of stroke patho-physiology have demonstrated the important role of endothelial intercellular adhesion molecule (ICAM-1) in targeting the leukocyte response to the ischemic brain region and transmigration of polymorphonuclears into the parenchyma. In this article, investigations suggesting beneficial effects of anti-adhesion therapies blocking the endothelial ICAM-1 or its counter-receptor CD11/CD18 on leukocytes are reviewed. This evidence should be viewed also in the context of human stroke, which has also recently been shown to overexpress ICAM-1 molecules on the infarcted endothelium. Well-tolerated monoclonal antibodies (mAb) blocking ICAM-1 might eventually be shown to possess therapeutic value acutely in clinical stroke victims, perhaps in combination with thrombolytic therapy.

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