| First Author | Hidalgo A | Year | 2007 |
| Journal | Immunity | Volume | 26 |
| Issue | 4 | Pages | 477-489 |
| PubMed ID | 17442598 | Mgi Jnum | J:123577 |
| Mgi Id | MGI:3718845 | Doi | 10.1016/j.immuni.2007.03.011 |
| Citation | Hidalgo A, et al. (2007) Complete identification of E-selectin ligands on neutrophils reveals distinct functions of PSGL-1, ESL-1, and CD44. Immunity 26(4):477-89 |
| abstractText | The selectins and their ligands are required for leukocyte extravasation during inflammation. Several glycoproteins have been suggested to bind to E-selectin in vitro, but the complete identification of its physiological ligands has remained elusive. Here, we showed that E-selectin ligand-1 (ESL-1), P-selectin glycoprotein ligand-1 (PSGL-1), and CD44 encompassed all endothelial-selectin ligand activity on neutrophils by using gene- and RNA-targeted loss of function. PSGL-1 played a major role in the initial leukocyte capture, whereas ESL-1 was critical for converting initial tethers into steady slow rolling. CD44 controlled rolling velocity and mediated E-selectin-dependent redistribution of PSGL-1 and L-selectin to a major pole on slowly rolling leukocytes through p38 signaling. These results suggest distinct and dynamic contributions of these three glycoproteins in selectin-mediated neutrophil adhesion and signaling. |
