AbstractHuman T lymphocyte adhesion to human endothelial cells is the initial event in T cell migration to areas of extravascular inflammation. The molecular basis for T cell‐endothelial cell adhesion was investigated using two different cell‐cell adhesion assays: (a) a fluorescein cell‐cell adhesion assay using non‐adherent endothelial cells and fluorescein‐labeled T lymphocytes, and (b) a radionuclide cell‐cell adhesion assay using adherent endothelial cells and51Cr‐labelled T cells. Both assay systems demonstrated comparable quantitative assessment of cell‐cell adhesions. The assays were performed at 22°C and adhesions were maximal at 30 min. The results of these adhesion assays confirmed previous reports that T cells adhere to endothelial cells. In addition, we have shown that T cells adhere only marginally to foreskin fibroblasts or bone marrow derived fibroblasts. T cell‐endothelial cell adhesions were significantly stronger than either monocytes or B lymphoblastoid cells adhesion to endothelial cells. To demonstrate the molecular mechanisms involved in regulating T cell‐endothelial cell adhesions, a panel of function‐associated monoclonal antibodies (MAb) were tested for their ability to inhibit T cell adhesion. MAb reactive with the leukocyte surface glycoprotein LFA‐1 signifi‐cantly inhibited T cell‐endothelial cell adhesions in both assay systems. In contrast, MAb directed at other surface antigens did not inhibit T cell adhesion. The involvement of the LFA‐1 glycoprotein in T lymphocyte adhesion to endothelial cells suggest that the LFA‐1 molecule may be important in the regu
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