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首页> 美国卫生研究院文献>Clinical and Experimental Immunology >Increased adhesion of human monocytes to IL-4-stimulated human venous endothelial cells via CD11/CD18 and very late antigen-4 (VLA-4)/vascular cell adhesion molecule-1 (VCAM-1)-dependent mechanisms.
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Increased adhesion of human monocytes to IL-4-stimulated human venous endothelial cells via CD11/CD18 and very late antigen-4 (VLA-4)/vascular cell adhesion molecule-1 (VCAM-1)-dependent mechanisms.

机译：人单核细胞通过CD11 / CD18和非常晚的抗原4（VLA-4）/血管细胞粘附分子1（VCAM-1）依赖性机制对IL-4刺激的人静脉内皮细胞的粘附增加。

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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.
机译：粘附分子在内皮细胞（EC）上的表达可被细胞因子上调或诱导。本研究的目的是研究IL-4对EC黏附分子表达和单核细胞对EC黏附的影响。流式细胞仪分析显示，IL-4刺激24小时后，EC上的VCAM-1表达上调，而E-选择素（以前称为内皮白细胞粘附分子1（ELAM-1））的表达未增强。 ，而胞间粘附分子1（ICAM-1）的作用则很小。在用IL-4刺激EC 24小时后，单核细胞对EC的粘附增加到最大值。 MoAb对整联蛋白β2亚基（CD18）的单核细胞涂层显着抑制了它们对IL-4刺激的EC的粘附；当单核细胞涂有抗CD18 MoAb与抗CD49d（VLA-4的α链）的MoAb结合时，发现最大的抑制作用，而当单核细胞仅涂有抗CD49d的MoAb时，没有发现抑制作用。当单独或联合使用抗ICAM-1或VCAM-1的MoAb包被IL-4刺激的EC时，单核细胞粘附未受到明显抑制。当除了用抗CD18的MoAb包被单核细胞外，用抗VCAM-1的MoAb包被的EC时，更大程度地抑制了单核细胞的粘附。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分子与尚不知道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。

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