INTERACTIONS OF HUMAN ALPHA BETA AND GAMMA/DELTA T-LYMPHOCYTE SUBSETSIN SHEAR-FLOW WITH E-SELECTIN AND P-SELECTIN/

We have compared the ability of human alpha/beta and gamma/delta T lym phocytes to adhere to selectin-bearing substrates, an interaction thou ght to be essential for homing and localization at sites of inflammati on. Both T cell populations form rolling adhesions on E- and P-selecti n substrates under physiologic now conditions. Although equivalent to alpha/beta T cells in binding to E-selectin, gamma/delta T cells demon strated greater ability to adhere to P-selectin that was purified or e xpressed on the surface of activated, adherent platelets. Under static conditions, 80% of gamma/delta T cells and 53% of alpha/beta T cells formed shear-resistant adhesions to P-selectin, whereas only 30% of ga mma/delta and alpha/beta T cells adhered to E-selectin. The enhanced a bility of gamma/delta T cells to adhere to P-selectin cannot be attrib uted to differences in expression of the P-selectin glycoprotein ligan d (PSGL-1), as all alpha/beta T cells versus similar to 75% of gamma/d elta T cells expressed PSGL-1. Both cell populations expressed a simil ar percentage of the carbohydrate antigens sialyl Lewis(x) and cutaneo us lymphocyte-associated antigen. Depletion of lymphocyte populations or T cell clones bearing these oligosaccharides with the monoclonal an tibody CSLEX-1 and HECA-452, respectively, resulted in a substantial r eduction in adhesion to E-selectin and slight reduction in adhesion to P-selectin under now conditions. Treatment of cells with an endopepti dase that selectively degrades O-sialomucins such as PSGL-1, abolished P-selectin but not E-selectin adhesion. Removal of terminal sialic ac ids with neuraminidase or protease treatment of cells abrogated cell a dhesion to both selectin substrates. These results provide direct evid ence for the presence of distinct E- and P-selectin ligands on T lymph ocytes and suggest that gamma/delta T cells may be preferentially recr uited to inflammatory sites during the early stages of an immune respo nse when P-selectin is upregulated.