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The Journal of Immunology, Vol 147, Issue 8 2565-2573, Copyright © 1991 by American Association of Immunologists
ARTICLES |
O Spertini, FW Luscinskas, GS Kansas, JM Munro, JD Griffin, MA Gimbrone Jr and TF Tedder
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115-6084.
The human lymphocyte homing receptor, LAM-1, mediates the adhesion of lymphocytes to specialized high endothelial venules (HEV) of peripheral lymph nodes. We now report that LAM-1 is also a major mediator of leukocyte attachment to activated human endothelium. In a novel adhesion assay, LAM-1 was shown to mediate approximately 50% of the adhesion of both lymphocytes and neutrophils to TNF-activated human umbilical vein endothelial cells at 4 degrees C. The contribution of LAM-1 to leukocyte adhesion was only detectable when the assays were carried out under rotating (nonstatic) conditions, suggesting that LAM- 1 is involved in the initial attachment of leukocytes to endothelium. In this assay at 37 degrees C, essentially all lymphocyte attachment to endothelium was mediated by LAM-1, VLA-4/VCAM-1, and the CD11/CD18 complex, whereas neutrophil attachment was mediated by LAM-1, endothelial-leukocyte adhesion molecule-1, and CD11/CD18. Thus, multiple receptors are necessary to promote optimal leukocyte adhesion to endothelium. LAM-1 also appeared to be involved in optimal neutrophil transendothelial migration using a videomicroscopic in vitro transmigration model system. LAM-1-dependent leukocyte adhesion required the induction and surface expression of a neuraminidase- sensitive molecule that was expressed for at least 24 h on activated endothelium. Expression of the LAM-1 ligand by endothelium was optimally induced by LPS and the proinflammatory cytokines TNF-alpha and IL-1 beta, whereas IFN-gamma and IL-4 induced lower levels of expression. The LAM-1 ligand on HEV and cytokine treated endothelium may be similar carbohydrate-containing molecules, because phosphomannan monoester core complex from yeast Hansenula hostii cell wall blocked binding of lymphocytes to both cell types, and identical epitopes on LAM-1-mediated lymphocyte attachment to HEV and activated endothelium. Thus, LAM-1 and its inducible endothelial ligand constitute a new pair of adhesion molecules that may regulate initial leukocyte/endothelial interactions at sites of inflammation.
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R.M. Nelson, A. Aruffo, S. Dolich, O. Cecconi, G. Mannori, and M.P. Bevilacqua Quantitative Determination of Selectin-Carbohydrate Interactions Cold Spring Harb Symp Quant Biol, January 1, 1992; 57(0): 271 - 279. [Abstract] [PDF]
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O. Dwir, Geoffrey. S. Kansas, and R. Alon An Activated L-selectin Mutant with Conserved Equilibrium Binding Properties but Enhanced Ligand Recognition under Shear Flow J. Biol. Chem., June 16, 2000; 275(25): 18682 - 18691. [Abstract] [Full Text] [PDF]
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P. Andre, O. Spertini, S. Guia, P. Rihet, F. Dignat-George, H. Brailly, J. Sampol, P. J. Anderson, and E. Vivier Modification of P-selectin glycoprotein ligand-1 with a natural killer cell-restricted sulfated lactosamine creates an alternate ligand for L-selectin PNAS, March 28, 2000; 97(7): 3400 - 3405. [Abstract] [Full Text] [PDF]
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F. S. Dhabhar, A. R. Satoskar, H. Bluethmann, J. R. David, and B. S. McEwen Stress-induced enhancement of skin immune function: A role for gamma interferon PNAS, March 14, 2000; 97(6): 2846 - 2851. [Abstract] [Full Text] [PDF]
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