JAM-C regulates unidirectional monocyte transendothelial migration in inflammation

PF Bradfield, C Scheiermann, S Nourshargh, C Ody, FW Luscinskas, George Rainger, Gerard Nash, M Miljkovic-Licina, M Aurrand-Lions, BA Imhof

Research output: Contribution to journalArticle

111 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)2545-2555
Number of pages11
JournalBlood
Volume110
Issue number7
DOIs
Publication statusPublished - 1 Oct 2007

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