Role of ICAM-1 in the Adherence of Human Neutrophils to Human Endothelial Cells In Vitro
The adherence of human neutrophils to endothelial cells and protein-coated foreign surfaces in vitro is significantly increased by chemotactic stimulation or exposure of the cells to secretagogues (1–7). The CD11b/ CD18 (Mac-1) heterodimer on the neutrophil’s surface appears to play a role as shown by the inhibitory effect of some monoclonal antibodies reactive with either CD1 lb or CD18 (4,5,8,9). Stimulation of endothelial cells with bacterial endotoxin (LPS) (4,10,11), interleukin-1 (IL-1) (4,12,13), tumor necrosis factor-α (TNF-α) (4,5,12–14), or lymphotoxin (LT) (13) increases the adherence of unstimulated neutrophils. In contrast to the rapid response following chemotactic stimulation of neutrophils, this increase is not evident until > 1 hour after stimulation, and protein synthesis is required. The specific CD11/CD18 heterodimers important to this cytokine-induced adherence have not been defined. We have recently obtained evidence that the CD18-dependent adherence of human neutrophils to cytokine-stimulated endothelial cells involves intercellular adherence molecule-1 (ICAM-1) expressed on the endothelial surface (7). In light of recent evidence that ICAM-1 (15,16) is a ligand for the CD11a/ CD18 (LFA-1) heterodimer (17,18), consideration was given to the possibility that LFA-1 contributes to the adherence of neutrophils to cytokine stimulated endothelial cells.
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