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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. This Article Full Text Full Text (PDF) Supplemental Figures and Videos All Versions of this Article: blood-2007-03-078733v1 110/7/2545    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bradfield, P. F. Articles by Imhof, B. A. Search for Related Content PubMed PubMed Citation Articles by Bradfield, P. F. Articles by Imhof, B. A. Related Collections Immunobiology Phagocytes Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. Shagdarsuren, Y. Djalali-Talab, M. Aurrand-Lions, K. Bidzhekov, E. A. Liehn, B. A. Imhof, C. Weber, and A. 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