The Junctional Adhesion Molecule-C Promotes Neutrophil Transendothelial Migration in Vitro and in Vivo*

摘要: The third member of the family junctional adhesion molecules (JAMs), JAM-3, also called JAM-C, was recently shown to be a novel counter-receptor on platelets for leukocyte β2-integrin Mac-1 (αMβ2, CD11b/CD18). Here, new functional aspects role endothelial cell JAM-C were investigated. Endothelial cells express which is predominantly localized within junctions at interendothelial contacts, since it codistributes with tight junction component, zonula occludens-1. Whereas does not participate in neutrophil cells, mediates transmigration Mac-1-dependent manner. In particular, inhibition significantly reduced transendothelial migration, and combination platelet/endothelial molecule-1 blockade almost completely abolished migration vitro. vivo, soluble mouse resulted 50% reduction emigration model acute thioglycollate-induced peritonitis. Thus, participates thereby provides molecular target antagonizing interactions between vascular that promote inflammatory pathologies.