The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/2/573/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 3, February 3, 1997 573-578

Brief Definitive Reports

P-Selectin Glycoprotein Ligand-1 (PSGL-1) on T Helper 1 but Not on T Helper 2 Cells Binds to P-Selectin and Supports Migration into Inflamed Skin

Eric Borges*, Wolfgang Tietz{ddagger}, Martin Steegmaier*, Thomas Moll*, Rupert Hallmann§, Alf Hamann{ddagger}, and Dietmar Vestweber*

From the * Institut für Zellbiologie, ZMBE, Universität Münster, Germany; {ddagger} Abteilung für Immunologie, Medizinische Klinik, Universitätskrankenhaus Eppendorf, Hamburg, Germany; § Institut für Exp. Medizin u. Bindegewebsforschung, Universität Erlangen-Nürnberg, Germany

We have shown recently that mouse Th1 cells but not Th2 cells are selectively recruited into inflamed sites of a delayed-type hypersensitivity (DTH) reaction of the skin. This migration was blocked by monoclonal antibodies (mAb) against P- and E-selectin. Here we show that Th1 cells bind to P-selectin via the P-selectin glycoprotein ligand-1 (PSGL-1). This is the only glycoprotein ligand that was detectable by affinity isolation with a P-selectin–Ig fusion protein. Binding of Th1 cells to P-selectin, as analyzed by flow cytometry and in cell adhesion assays, was completely blocked by antibodies against PSGL-1. The same antibodies blocked partially the migration of Th1 cells into cutaneous DTH reactions. This blocking activity, in combination with that of a mAb against E-selectin, was additive. PSGL-1 on Th2 cells, although expressed at similar levels as on Th1 cells, did not support binding to P-selectin. Thus, the P-selectin–binding form of PSGL-1 distinguishes Th1 cells from Th2 cells. Furthermore, PSGL-1 is relevant for the entry of Th1 cells into inflamed areas of the skin. This is the first demonstration for the importance of PSGL-1 for mouse leukocyte recruitment in vivo.

Address correspondence to Dietmar Vestweber, Institute of Cell Biology, ZMBE, Technologiehof, Mendelstr. 11, D-48149 Münster, Germany.

This work was supported by grants from the Deutsche Forschungsgemeinschaft to D. Vestweber, R. Hallmann, and A. Hamann and from the Mildred Scheel Stiftung to A. Hamann.


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