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dc.contributor.authorWoodfin, Aen_US
dc.contributor.authorVoisin, MBen_US
dc.contributor.authorBeyrau, Men_US
dc.contributor.authorColom, Ben_US
dc.contributor.authorCaille, Den_US
dc.contributor.authorDiapouli, FMen_US
dc.contributor.authorNash, GBen_US
dc.contributor.authorChavakis, Ten_US
dc.contributor.authorAlbelda, SMen_US
dc.contributor.authorRainger, GEen_US
dc.contributor.authorMeda, Pen_US
dc.contributor.authorImhof, BAen_US
dc.contributor.authorNourshargh, Sen_US
dc.date.accessioned2017-03-03T16:40:16Z
dc.date.available2011-05-26en_US
dc.date.issued2011-08en_US
dc.date.submitted2017-01-03T14:54:21.599Z
dc.identifier.issn1529-2908en_US
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/19663
dc.description.abstractThe 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.
dc.format.extent761 - U145en_US
dc.relation.ispartofNAT IMMUNOLen_US
dc.subjectGREEN FLUORESCENT PROTEINen_US
dc.subjectTRANSCELLULAR MIGRATIONen_US
dc.subjectLEUKOCYTE TRANSMIGRATIONen_US
dc.subjectINFLAMMATIONen_US
dc.subjectEXTRAVASATIONen_US
dc.subjectPERMEABILITYen_US
dc.subjectENDOTHELIUMen_US
dc.subjectRECRUITMENTen_US
dc.subjectINSERTIONen_US
dc.subjectCONTACTSen_US
dc.titleThe junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivoen_US
dc.typeArticle
dc.rights.holder© 2022 Springer Nature Limited
dc.identifier.doi10.1038/ni.2062en_US
pubs.issue8en_US
pubs.notesNot knownen_US
pubs.volume12en_US
qmul.funderAn investigation into the molecular and cellular mechanisms involved in mediating neutrophil and monocyte transmigration in vivo::Wellcome Trusten_US


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