The expanding role of α2-3 sialylation for leukocyte trafficking in vivo.

The ability of leukocytes to navigate through the different body compartments is an essential component for functioning immune defense and surveillance systems. In order to exit the blood circulation, leukocytes follow distinct recruitment steps, including capture of free-flowing leukocytes to, and rolling along, the vessel wall; firm leukocyte arrest on the endothelial lining; and postarrest modifications (spreading and crawling), which prepare the leukocyte for transmigration through the vascular wall. Post-translational glycosylation (including sialylation) has been known for many years to be functionally relevant for selectin ligands and, hence, selectin-mediated capture and rolling. Recently, sialylation by the α2-3 sialyltransferase ST3Gal-IV was identified to significantly influence chemokine-triggered firm leukocyte arrest, expanding the role of α2-3 sialylation from leukocyte rolling to subsequent chemokine-triggered leukocyte arrest. These findings make ST3Gal-IV an interesting drug target for modulating leukocyte trafficking in human disorders, including autoimmune diseases and cancer.