ICAM1 and stroke disorder: Furthermore, although some animal experiments targeting adhesion molecules mediating the multi-step PMN migration across inflamed microvessels have shown reduced infarct size [25], clinical trials targeting PMN adhesion to endothelial ICAM-1 [9, 36, 47] or aiming at preventing PMN infiltration into the brain by neutralizing the αMβ2-integrin (CD11b/CD18) [54] have failed to alleviate stroke severity, suggesting that the mode of PMN action requires reassessment.