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* Department of Veterinary and Biomedical Sciences, University of Minnesota, St. Paul, MN 55108;
Department of Pathology, Harvard Medical School, and
Joint Program in Transfusion Medicine, Children’s Hospital Boston, Boston, MA 02115; and
Minneapolis Department of Veterans Affairs Medical Center, Minneapolis, MN 55417
T cells use the vascular adhesion molecules E- and P-selectin to enter inflamed skin. Previous studies have indicated the possibility for diversity in the synthesis of E- and P-selectin glycan ligands by activated T cells due to their different requirements for the O-glycan branching enzyme core 2 
1,6-N-acetylglucosaminyltransferase I and its independent regulation. It is known that T cell staining by the mAb HECA-452 (referred to as cutaneous lymphocyte-associated Ag (CLA) T cells) correlates with E-selectin binding, yet whether these cells uniformly bind P-selectin is less clear. The mAb CHO-131 and P-selectin binding require a glycan moiety consisting of a sialylated and fucosylated oligosaccharide properly positioned on a core-2 O-glycan. Interestingly, CHO-131 stains a subset of CLA+ T cells. A direct comparison of the selectin binding capacity of CHO-131+ and CHO-131– CLA+ T cells revealed a significantly greater P-selectin, but not E-selectin, binding activity by the former subset. Based on the expression of homing and central and effector memory cell markers, CHO-131+ and CHO-131– CLA+ T cells have an overlapping skin-tropic and memory phenotype. CHO-131+ T cells were considerably enriched in psoriatic skin, yet, unlike the peripheral blood of healthy individuals, HECA-452 and CHO-131 stained a similar proportion of T cells in the cutaneous lesions, indicating an accumulation advantage by CHO-131+ T cells. We conclude that the CHO-131+CLA+ T cell subset is enriched in P-selectin binding cells. These findings should provide new insights into the regulation and function of skin homing T cells.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This study was supported by National Institutes of Health Grants HL61613, AR049333 (to B.W.), and AI46784 (to J.J.C.).
2 Current addresses: Department of Dermatology, Brigham and Women’s Hospital and Departments of Dermatology and Pathology, Harvard Medical School, Boston, MA 02115.
3 Address correspondence and reprint requests to Dr. Bruce Walcheck, University of Minnesota, 295j Animal Science/Veterinary Medicine Building, 1988 Fitch Avenue, St. Paul, MN 55108. E-mail address: walch003{at}umn.edu
4 Abbreviations used in this paper: CLA, cutaneous lymphocyte-associated Ag; sLeX, sialyl-LewisX; FucT-VII, 
1,3-fucosyltransferase VII; C2GlcNAcT, core 2 1,6-N-acetylglucosaminyltransferase; PSGL-1, P-selectin glycoprotein ligand-1; C2-O-sLeX, core 2 O-glycan terminated with sialyl-LewisX.
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