IL-4, but not tumor necrosis factor-alpha, increases endothelial cell adhesiveness for lymphocytes by activating a cAMP-dependent pathway.

摘要: IL-4 and TNF-alpha increase endothelial cell adhesiveness for PBL by promoting the expression of adhesion molecules. We investigated intracellular cAMP involvement in increased adhesivity induced or TNF-alpha. showed that both cells (EC). Furthermore, dibutyryl-cAMP forskolin (which cAMP) basic EC PBL. The co-stimulation with elevating agents TNF-alpha, but not IL-4, resulted an additive adhesiveness. 2',5' dideoxyadenosine, inhibitor adenylate cyclase, decreased to IL-4- TNF-alpha-treated EC. Similarly, HA1004, a protein kinase A inhibitor, totally reversed effect on adhesiveness, whereas H7, C did antagonise cytokine-enhanced adhesivity. These results indicate uses cAMP-dependent pathway adhesion. we elevation induce vascular molecule 1, only identified indicating rise promotes as yet unidentified pathway. Our show increases through activation