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Publication : JAM-C regulates unidirectional monocyte transendothelial migration in inflammation.

First Author  Bradfield PF Year  2007
Journal  Blood Volume  110
Issue  7 Pages  2545-55
PubMed ID  17625065 Mgi Jnum  J:147010
Mgi Id  MGI:3839081 Doi  10.1182/blood-2007-03-078733
Citation  Bradfield PF, et al. (2007) JAM-C regulates unidirectional monocyte transendothelial migration in inflammation. Blood 110(7):2545-55
abstractText  Monocyte recruitment from the vasculature involves sequential engagement of multiple receptors, culminating in transendothelial migration and extravasation. Junctional adhesion molecule-C (JAM-C) is localized at endothelial intercellular junctions and plays a role in monocyte transmigration. Here, we show that blockade of JAM-B/-C interaction reduced monocyte numbers in the extravascular compartment through increased reverse transmigration rather than by reduced transmigration. This was confirmed in vivo, showing that an anti-JAM-C antibody reduced the number of monocytes in inflammatory tissue and increased the number of monocytes with a reverse-transmigratory phenotype in the peripheral blood. All together, our results suggest a novel mechanism of reducing accumulation of monocytes at inflammation sites by disruption of JAM-C-mediated monocyte retention.
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