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JAM-C regulates unidirectional monocyte transendothelial migration in inflammation

Bradfield, Paul F.
Scheiermann, Christoph
Nourshargh, Sussan
Luscinskas, F. W.
Rainger, G. E.
Nash, G. B.
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Published in Blood. 2007, vol. 110, no. 7, p. 2545-2555
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.
Keywords AnimalsAntibodies/immunologyBlood Platelets/metabolismCell AdhesionCell Adhesion Molecules/genetics/immunology/ metabolismCell MovementCells, CulturedEndothelial Cells/metabolismHumansInflammation/metabolism/pathologyMiceMice, TransgenicMonocytes/ cytology/ metabolismPhenotype
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PMID: 17625065
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