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. |