The alpha(1,3)fucosyltransferases FucT-IV and FucT-VII exert collaborativecontrol over selectin-dependent leukocyte recruitment and lymphocyte homing

E-, P-, and L-selectin counterreceptor activities, leukocyte trafficking, a nd lymphocyte homing are controlled prominently but incompletely by alpha ( 1,3)fucosyltransferase FucT-VII-dependent fucosylation. Molecular determina nts for FucT-VII-independent leukocyte trafficking are not defined, and evi dence for contributions by or requirements for other FucTs in leukocyte rec ruitment is contradictory and incomplete. We show here that inflammation-de pendent leukocyte recruitment retained in FucT-VII deficiency is extinguish ed in FucT-1V(-/-)/FucT-VII-/- mice. Double deficiency yields an extreme le ukocytosis characterized by decreased neutrophil turnover and increased neu trophil production. FucT-IV also contributes to HEV-born L-selectin ligands , since lymphocyte homing retained in FucT-VII-/- mice is revoked in FucT-I V-/-/FucT-VII-/- mice. These observations reveal essential FucT-IV-dependen t contributions to E-, P-, and L-selectin ligand synthesis and to the contr ol of leukocyte recruitment and lymphocyte homing.