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Woodfin, A.* ; Voisin, M.B.* ; Beyrau, M.* ; Colom, B.* ; Caille, D.* ; Diapouli, F.M.* ; Nash, G.B.* ; Chavakis, T.* ; Albelda, S.M.* ; Rainger, G.E.* ; Meda, P.* ; Imhof, B.A.* ; Nourshargh, S.*

The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo.

Nat. Immunol. 12, 761-769 (2011)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 1529-2908
e-ISSN 1529-2916
Zeitschrift Nature Immunology
Quellenangaben Band: 12, Heft: 8, Seiten: 761-769 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Pancreatic Beta Cell Research (IPI)