ICAM-1 as a potential target for treatments blocking the host response in stroke.
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 pathophysiology 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 CDII/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.
Department of Neurology, University of Helsinki, Finland.
P J
PJ
Lindsherg
D002561:Cerebrovascular Disorders / Q000628:therapy*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology*; D007962:Leukocytes / Q000502:physiology*; D008833:Microcirculation / Q000502:physiology; D009474:Neurons / Q000502:physiology*
D018799:Intercellular Adhesion Molecule-1