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JAM-C regulates unidirectional monocyte transendothelial migration in inflammation.

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.

SUBMITTER: Bradfield PF

PROVIDER: S-EPMC1988941 | biostudies-literature | 2007 Oct

REPOSITORIES: biostudies-literature

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JAM-C regulates unidirectional monocyte transendothelial migration in inflammation.

Bradfield Paul F PF Scheiermann Christoph C Nourshargh Sussan S Ody Christiane C Luscinskas Francis W FW Rainger G Ed GE Nash Gerard B GB Miljkovic-Licina Marijana M Aurrand-Lions Michel M Imhof Beat A BA

Blood 20070711 7

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 confirme ...[more]

PMID: 17625065

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