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J. Exp. Med.,
Volume 189, Number 2, January 18, 1999 241-252
By


From the * Department of Immunology, Duke University Medical Center, Durham, North Carolina
27710; and L-selectin mediates leukocyte rolling on vascular endothelium during inflammation. Although
vascular endothelium can be activated with inflammatory cytokines to express functional L-selectin ligands, these ligands have not been well characterized. In this study, fucosyltransferase VII
cDNA (Fuc-TVII) transfection of the EA.hy926 human vascular endothelial cell line (926-FtVII) induced functional L-selectin ligand expression and expression of sialyl Lewisx (sLex), as
defined by HECA-452 (cutaneous lymphocyte antigen; CLA) and CSLEX-1 mAbs. Cytokine
activation of human umbilical vein endothelial cells (HUVEC) also induced functional L-selectin ligand expression, with increased CLA expression and Fuc-TVII transcription. The majority
of L-selectin-dependent lymphocyte attachment to activated HUVEC and 926-FtVII cells was
blocked specifically by treating the endothelial cells with the HECA-452 mAb, but not the
CSLEX-1 mAb. CLA-bearing ligands on vascular endothelium also required sulfation and appropriate molecular scaffolds for functional activity, but were distinct from the L-selectin ligands
previously identified by the MECA-79 mAb. These findings demonstrate that the HECA-452-
defined antigen, CLA, is an essential carbohydrate component of vascular L-selectin ligands.
Vascular Research Division, Department of Pathology, Brigham and Women's Hospital
and Harvard Medical School, Boston, Massachusetts 02160
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