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Blood. 2007 Oct 1;110(7):2545-55. Epub 2007 Jul 11.

JAM-C regulates unidirectional monocyte transendothelial migration in inflammation.

Author information

1
Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland.

Abstract

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.

PMID:
17625065
PMCID:
PMC1988941
DOI:
10.1182/blood-2007-03-078733
[Indexed for MEDLINE]
Free PMC Article

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