Advertisement
Research Article Free access | 10.1172/JCI114668
Department of Medicine, University of Washington, Seattle 98195.
Find articles by Schwartz, B. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington, Seattle 98195.
Find articles by Wayner, E. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington, Seattle 98195.
Find articles by Carlos, T. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington, Seattle 98195.
Find articles by Ochs, H. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Washington, Seattle 98195.
Find articles by Harlan, J. in: JCI | PubMed | Google Scholar
Published June 1, 1990 - More info
Patients with the severe form of leukocyte adhesion deficiency syndrome do not express the CD11/CD18 adhesion complex on any of their leukocytes. Nevertheless, their lymphocytes, unlike their phagocytes, emigrate to extravascular sites of inflammation, demonstrating that surface proteins other than CD11/CD18 can mediate lymphocyte adherence to endothelium. Using a B-lymphoblastoid cell line (B-LCL) established from a CD11/CD18-deficient patient and cultured human umbilical vein endothelial cells (HEC), we investigated the CD11/CD18-independent mechanism(s) of lymphocyte adherence to endothelium. Monoclonal antibodies directed to the alpha 4 polypeptide (CD49d) and the beta 1 polypeptide (CD29) of the lymphocyte VLA-4 integrin receptor (CD49d/CD29), and to vascular cell adhesion molecule-1 (VCAM-1) on the endothelial cell significantly inhibited the adherence of the CD11/CD18-deficient B-LCL to untreated HEC and to HEC treated with recombinant human tumor necrosis factor-alpha. We suggest that the interaction of the lymphocyte receptor VLA-4 with the endothelial ligand VCAM-1 induced by cytokines at sites of inflammation or immune reaction represents a CD11/CD18-independent pathway of lymphocyte emigration.
Click on an image below to see the page. View PDF of the complete article