Abstract
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.
Original language | English (US) |
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Pages (from-to) | 477-489 |
Number of pages | 13 |
Journal | Immunity |
Volume | 26 |
Issue number | 4 |
DOIs | |
State | Published - Apr 27 2007 |
Externally published | Yes |
Keywords
- CELL_IMMUNO
- MOL_IMMUNO
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Infectious Diseases