Verdegaal E M, Beekhuizen H, Blokland I, van Furth R
Department of Infectious Diseases, University Hospital, Leiden, The Netherlands.
Clin Exp Immunol. 1993 Aug;93(2):292-8. doi: 10.1111/j.1365-2249.1993.tb07982.x.
Expression of adhesion molecules on endothelial cells (EC) can be up-regulated or induced by cytokines. The aim of the present study was to investigate the effect of IL-4 on both the expression of adhesion molecules on EC and monocyte adhesion to EC. Flow cytometric analysis showed that VCAM-1 expression on EC was up-regulated after stimulation with IL-4 for 24 h, whereas the expression of E-selectin (formerly called endothelial leucocyte adhesion molecule-1 (ELAM-1)) was not enhanced, and that of intercellular adhesion molecule-1 (ICAM-1) only slightly. The adhesion of monocytes to EC increased to maximum values upon stimulation of EC with IL-4 for 24 h. Coating of monocytes with MoAb against the integrin beta 2-subunit (CD18) significantly inhibited their adhesion to IL-4-stimulated EC; maximal inhibition was found when monocytes were coated with anti-CD18 MoAb in combination with MoAb against CD49d (the alpha-chain of VLA-4), whereas no inhibition was found when monocytes were coated only with MoAb against CD49d. Monocyte adhesion was not significantly inhibited when IL-4-stimulated EC were coated with MoAbs against ICAM-1 or VCAM-1 alone or in combination. Adhesion of monocytes was inhibited to a greater extent when in addition to coating of monocytes with MoAb against CD18 the EC were coated with MoAb against VCAM-1. From these results we conclude that monocytes bind to IL-4-stimulated EC via interaction of CD11/CD18 molecules on the monocytes with an as yet unknown endothelial ligand, and interaction of VLA-4 on monocytes with VCAM-1 on EC.
细胞因子可上调或诱导内皮细胞（EC）上黏附分子的表达。本研究的目的是探讨白细胞介素-4（IL-4）对EC上黏附分子表达及单核细胞与EC黏附的影响。流式细胞术分析显示，用IL-4刺激EC 24小时后，VCAM-1在EC上的表达上调，而E-选择素（原称为内皮白细胞黏附分子-1（ELAM-1））的表达未增强，细胞间黏附分子-1（ICAM-1）的表达仅略有增加。用IL-4刺激EC 24小时后，单核细胞与EC的黏附增加至最大值。用抗整合素β2亚基（CD18）的单克隆抗体（MoAb）包被单核细胞可显著抑制其与IL-4刺激的EC的黏附；当单核细胞用抗CD18 MoAb与抗CD49d（VLA-4的α链）的MoAb联合包被时，发现最大抑制作用，而当单核细胞仅用抗CD49d的MoAb包被时未发现抑制作用。当单独或联合用抗ICAM-1或VCAM-1的MoAb包被IL-4刺激的EC时，单核细胞黏附未受到显著抑制。当除了用抗CD18的MoAb包被单核细胞外，还用抗VCAM-1的MoAb包被EC时，单核细胞的黏附受到更大程度的抑制。从这些结果我们得出结论，单核细胞通过单核细胞上的CD11/CD18分子与一种尚未明确的内皮配体相互作用，以及单核细胞上的VLA-4与EC上的VCAM-1相互作用，与IL-4刺激的EC结合。
