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 Blood, 1 October 2007, Vol. 110, No. 7, pp. 2545-2555.
Prepublished online as a Blood First Edition Paper on July 11, 2007; DOI 10.1182/blood-2007-03-078733.

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IMMUNOBIOLOGY

JAM-C regulates unidirectional monocyte transendothelial migration in inflammation

Paul F. Bradfield1, Christoph Scheiermann2, Sussan Nourshargh2, Christiane Ody1, Francis W. Luscinskas3, G. Ed Rainger4, Gerard B. Nash4, Marijana Miljkovic-Licina1, Michel Aurrand-Lions1, and Beat A. Imhof1

1 Department of Pathology and Immunology, University Medical Centre, Geneva, Switzerland; 2 Faculty of Medicine, Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London, United Kingdom; 3 Department of Pathology, Center for Excellence in Vascular Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; 4 The Centre for Cardiovascular Sciences, Centre for Immune Regulation and the Medical Research Council (MRC) Centre, The University of Birmingham, Birmingham, United Kingdom

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.


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