E-selectin

E-selectin, also called as CD62, is not present on the unstimulated endothelial cells but expressed exclusively by activated endothelium [BSGS89]. Most of the evidence that implicates E-selectin as a mediator of leucocyte rolling in inflamed microvasculature is inferred from in vitro studies [LS93,AKM$^+$93]. Induction of the E-selectin gene in cultured endothelial cells by inflammatory stimuli, such as endotoxin, IL-1$\beta$ or TNF- induces gene transcription and surface expression of the E-selectin protein that is detectable within an hour of endothelial cells activation. E-selectin expression is maximal at 4 to 8 hours after endothelial activation but then gradually disappears from the endothelial cell surface within 12 to 24 hours [McE91]. E-selectin mediated neutrophil adhesion is CD11/CD18 independent. Monoclonal antibodies directed against L-selectin and E-selectin inhibit neutrophil adherence to endothelial cell stimulated by cytokines for 4 hours but do not affect adherence to endothelium for 24 hours [KWJ$^+$91]. These findings are consistent with the kinetics of E-selectin expression on activated endothelial cells and suggest that E-selectin uses L-selectin as a counter-receptor. When neutrophils bind to E-selectin, there is an increase in binding avidity of CD11/CD18 [LLR$^+$91].