Surface molecules involved in the adherence of recombinant interferon-gamma (rIFN-γ)-stimulated human monocytes to vascular endothelial cells

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Abstract
SUMMARY: During an inflammatory reaction, an increased number of circulating monocytes adhere to the endothelial cells (EC) of the vessel wall. This process is mediated by molecules located on the surface of monocytes and EC. Locally released Inflammatory mediators can modulate monocyte EC interaction. In an earlier study we reported that stimulation of monolayers of cultured venous EC with rIFN-γ enhanced their adhesiveness for monocytes. The aim of the present study was to investigate the effect of rIFN-γ on peripheral blood monocytes with regard to the expression of surface molecules and the binding to non-stimulated or cytokine-stimulated EC. Flow cytometric analysis demonstrated that monocytes stimulated with 500 U/ml rIFN-γ for 24 h showed increased expression of CR3 (CDIIb;CD18), p150,95 (CD11c/CD18) and Fc-γ (CD64); the expression of LFA-1 (CD11 la/CD18). L-selectin, CD14 and VLA-4 (CD49d/CD29) did not change or was slightly reduced. Upon stimulation with rIFN-γ monocytes showed an enhanced binding to both nonstimulated or rIFN-γ-stimulated EC. This was even more pronounced when EC had been stimulated with rIL-lα for 24 h. The increased binding of rIFN-γstimulated monocytes to rIL-lα-stimulated EC was further analysed. Studies with MoAbs against adhesion molecules on monocytes revealed that the binding of rIFN-γ-stimulated monocytes, hut not that of non-stimulated monocytes, to rIL-lα stimulated EC was inhibited by about 30–60% with MoAbs against CD11a. CDllb, CD18, L-selectin or CD14. MoAbs againsi CD11c or CD49d had little or no effect. From these results, we conclude that exposure of monocytes to rIFN-γ enhances their adhesiveness to cytokine-stimulated EC by a mechanism which involves CD11a/CD18, CD11b/CD18, CD14 and L-selectin on monocytes.