| First Author | Woodfin A | Year | 2011 |
| Journal | Nat Immunol | Volume | 12 |
| Issue | 8 | Pages | 761-9 |
| PubMed ID | 21706006 | Mgi Jnum | J:174437 |
| Mgi Id | MGI:5086038 | Doi | 10.1038/ni.2062 |
| Citation | Woodfin A, et al. (2011) The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo. Nat Immunol 12(8):761-9 |
| abstractText | The migration of neutrophils into inflamed tissues is a fundamental component of innate immunity. A decisive step in this process is the polarized migration of blood neutrophils through endothelial cells (ECs) lining the venular lumen (transendothelial migration (TEM)) in a luminal-to-abluminal direction. By real-time confocal imaging, we found that neutrophils had disrupted polarized TEM ('hesitant' and 'reverse') in vivo. We noted these events in inflammation after ischemia-reperfusion injury, characterized by lower expression of junctional adhesion molecule C (JAM-C) at EC junctions, and they were enhanced by blockade or genetic deletion of JAM-C in ECs. Our results identify JAM-C as a key regulator of polarized neutrophil TEM in vivo and suggest that reverse TEM of neutrophils can contribute to the dissemination of systemic inflammation. |
