THE ALPHA(1,3)FUCOSYLTRANSFERASE FUC-TVII CONTROLS LEUKOCYTE TRAFFICKING THROUGH AN ESSENTIAL ROLE IN L-SELECTIN, E-SELECTIN, AND P-SELECTIN LIGAND BIOSYNTHESIS

alpha(1,3)Fucosylated oligosaccharides represent components of leukocy te counterreceptors for E- and P-selectins and of L-selectin ligands e xpressed by lymph node high endothelial venules (HEV). The identity of the alpha(1,3)fucosyltransferase(s) required for their expression has been uncertain, as has a requirement for alpha(1,3)fucosylation in HE V L-selectin ligand activity. We demonstrate here that mice deficient in alpha(1,3)fucosyltransferase Fuc-TVII exhibit a leukocyte adhesion deficiency characterized by absent leukocyte E- and P-selectin ligand activity and deficient HEV L-selectin ligand activity. Selectin ligand deficiency is distinguished by blood leukocytosis, impaired leukocyte extravasation in inflammation, and faulty lymphocyte homing. These ob servations demonstrate an essential role for Fuc-TVII in E-, P-, and L -selectin ligand biosynthesis and imply that this locus can control le ukocyte trafficking in health and disease.