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Prepublished online as a Blood First Edition Paper on April 30, 2002; DOI 10.1182/blood-2001-11-0098. This Article Full Text Full Text (PDF) All Versions of this Article: 2001-11-0098v1 100/7/2479    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 Johnson-Léger, C. A. Articles by Imhof, B. A. Search for Related Content PubMed PubMed Citation Articles by Johnson-Léger, C. A. Articles by Imhof, B. A. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 October 2002, Vol. 100, No. 7, pp. 2479-2486 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Junctional adhesion molecule-2 (JAM-2) promotes lymphocyte transendothelial migration Caroline A. Johnson-Léger, Michel Aurrand-Lions, Nicola Beltraminelli, Nicolas Fasel, and Beat A. Imhof From the Department of Pathology, University Medical Centre, 1, Rue Michel-Servet, Geneva, Switzerland; RMF Dictagene, Epalinges, Switzerland; and Institute of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland. The molecular mechanisms underlying lymphocyte extravasation remain poorly characterized. We have recently identified junctional adhesion molecule-2 (JAM-2), and have shown that antibodies to JAM-2 stain high endothelial venules (HEVs) within lymph nodes and Peyer patches of adult mice. Here we show that mouse lymphocytes migrate in greater numbers across monolayers of endothelioma cells transfected with JAM-2. The significance of these findings to an understanding of both normal and pathologic lymphocyte extravasation prompted us to clone the human homologue of JAM-2. We herein demonstrate that an anti-JAM-2 antibody, or a soluble JAM-2 molecule, blocks the transmigration of primary human peripheral blood leukocytes across human umbilical vein endothelial cells expressing endogenous JAM-2. Furthermore, we show that JAM-2 is expressed on HEVs in human tonsil and on a subset of human leukocytes, suggesting that JAM-2 plays a central role in the regulation of transendothelial migration. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. A. Mendes-da-Cruz, S. Smaniotto, A. C. Keller, M. Dardenne, and W. Savino Multivectorial Abnormal Cell Migration in the NOD Mouse Thymus J. Immunol., April 1, 2008; 180(7): 4639 - 4647. [Abstract] [Full Text] [PDF] Y. Sugano, M. Takeuchi, A. Hirata, H. Matsushita, T. Kitamura, M. Tanaka, and A. Miyajima Junctional adhesion molecule-A, JAM-A, is a novel cell-surface marker for long-term repopulating hematopoietic stem cells Blood, February 1, 2008; 111(3): 1167 - 1172. [Abstract] [Full Text] [PDF] M. Nakhaei-Nejad, A. M. Hussain, Q.-X. Zhang, and A. G. 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	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020