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The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo.
Nat. Immunol. 12, 761-769 (2011)
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.
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Publication type
Article: Journal article
Document type
Scientific Article
Language
english
Publication Year
2011
HGF-reported in Year
0
ISSN (print) / ISBN
1529-2908
e-ISSN
1529-2916
Journal
Nature Immunology
Quellenangaben
Volume: 12,
Issue: 8,
Pages: 761-769
Publisher
Nature Publishing Group
Reviewing status
Peer reviewed
Institute(s)
Institute of Pancreatic Islet Research (IPI)
PubMed ID
21706006
DOI
10.1038/ni.2062
Erfassungsdatum
2011-12-31