A cloned CD15s-negative variant of HL60 cells is deficient in expression of FUT7 and does not adhere to cytokine-stimulated endothelial cells

The initial steps of leukocyte adhesion depend on selectin/ligand interacti ons. Surface ligands on leukocytes are often modified by addition of the si alyl Lewis x (CD15s) determinant. Biosynthesis of CD15s is dependent upon a lpha(2,3)sialyltransferases and alpha(1,3)fucosyl-transferases. We report t he isolation of an HL60 cell line variant, HL60A2, that no longer expresses CD15s. HL60A2 cells do not adhere to cytokine-stimulated endothelial cells . Enzymatic assays reveal that this cell line has normal alpha(2,3)sialyltr ansferase activity but is deficient in the alpha(1,3)fucosyltransferase res ponsible for biosynthesis of CD15s (FUT7). The fucosyltransferase that cons tructs the non-sialylated antigen, Lewis x (CD15), is expressed at high lev els (FUT4). Transcript analyses show that FUT7 and FUT4 are inversely expre ssed in HL60 and variant cell lines. HL60A2 cells provide a tool to study t he regulation of selectin ligands and corresponding human fucosyltransferas e genes.