J. Cell Biol., Volume 142, Number 1, July 13, 1998 117-127

Junctional Adhesion Molecule, a Novel Member of the Immunoglobulin Superfamily That Distributes at Intercellular Junctions and Modulates Monocyte Transmigration

Inés Martìn-Padura,^* Susan Lostaglio,^* Markus Schneemann, Lisa Williams, Maria Romano,^* Paolo Fruscella,^* Carla Panzeri,^§ Antonella Stoppacciaro, Luigi Ruco, Antonello Villa,^§ David Simmons, and Elisabetta Dejana^*

^* Istituto di Ricerche Farmacologiche Mario Negri, 20157 Milano, Italy;  Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Headington, Oxford, OX3 9DU, United Kingdom; ^§ Dipartimento di Farmacologia, Universita degli Studi di Milano, and DIBIT, Milano, Italy 20129; and  Universita' degli Studi La Sapienza, Dipartimento di Medicina Sperimentale e Patologia, 00161 Roma, Italy

Tight junctions are the most apical components of endothelial and epithelial intercellular cleft. In the endothelium these structures play an important role in the control of paracellular permeability to circulating cells and solutes. The only known integral membrane protein localized at sites of membrane-membrane interaction of tight junctions is occludin, which is linked inside the cells to a complex network of cytoskeletal and signaling proteins. We report here the identification of a novel protein (junctional adhesion molecule [JAM]) that is selectively concentrated at intercellular junctions of endothelial and epithelial cells of different origins. Confocal and immunoelectron microscopy shows that JAM codistributes with tight junction components at the apical region of the intercellular cleft. A cDNA clone encoding JAM defines a novel immunoglobulin gene superfamily member that consists of two V-type Ig domains. An mAb directed to JAM (BV11) was found to inhibit spontaneous and chemokine-induced monocyte transmigration through an endothelial cell monolayer in vitro. Systemic treatment of mice with BV11 mAb blocked monocyte infiltration upon chemokine administration in subcutaneous air pouches. Thus, JAM is a new component of endothelial and epithelial junctions that play a role in regulating monocyte transmigration.

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• Aurrand-Lions, M., Lamagna, C., Dangerfield, J. P., Wang, S., Herrera, P., Nourshargh, S., Imhof, B. A. (2005). Junctional Adhesion Molecule-C Regulates the Early Influx of Leukocytes into Tissues during Inflammation. J. Immunol. 174: 6406-6415 [Abstract] [Full Text]  
• Miyamoto, T., Morita, K., Takemoto, D., Takeuchi, K., Kitano, Y., Miyakawa, T., Nakayama, K., Okamura, Y., Sasaki, H., Miyachi, Y., Furuse, M., Tsukita, S. (2005). Tight junctions in Schwann cells of peripheral myelinated axons: a lesson from claudin-19-deficient mice. JCB 169: 527-538 [Abstract] [Full Text]  
• Ostermann, G., Fraemohs, L., Baltus, T., Schober, A., Lietz, M., Zernecke, A., Liehn, E. A., Weber, C. (2005). Involvement of JAM-A in Mononuclear Cell Recruitment on Inflamed or Atherosclerotic Endothelium: Inhibition by Soluble JAM-A. Arterioscler. Thromb. Vasc. Bio. 25: 729-735 [Abstract] [Full Text]  
• Mandell, K. J., Babbin, B. A., Nusrat, A., Parkos, C. A. (2005). Junctional Adhesion Molecule 1 Regulates Epithelial Cell Morphology through Effects on {beta}1 Integrins and Rap1 Activity. J. Biol. Chem. 280: 11665-11674 [Abstract] [Full Text]  
• Watts, G. M., Beurskens, F. J. M., Martin-Padura, I., Ballantyne, C. M., Klickstein, L. B., Brenner, M. B., Lee, D. M. (2005). Manifestations of Inflammatory Arthritis Are Critically Dependent on LFA-1. J. Immunol. 174: 3668-3675 [Abstract] [Full Text]  
• Yun, P. L. W., Decarlo, A. A., Chapple, C. C., Hunter, N. (2005). Functional Implication of the Hydrolysis of Platelet Endothelial Cell Adhesion Molecule 1 (CD31) by Gingipains of Porphyromonas gingivalis for the Pathology of Periodontal Disease. Infect. Immun. 73: 1386-1398 [Abstract] [Full Text]  
• Kondoh, M., Masuyama, A., Takahashi, A., Asano, N., Mizuguchi, H., Koizumi, N., Fujii, M., Hayakawa, T., Horiguchi, Y., Watanbe, Y. (2005). A Novel Strategy for the Enhancement of Drug Absorption Using a Claudin Modulator. Mol. Pharmacol. 67: 749-756 [Abstract] [Full Text]  
• de Noronha, S., Hardy, S., Sinclair, J., Blundell, M. P., Strid, J., Schulz, O., Zwirner, J., Jones, G. E., Katz, D. R., Kinnon, C., Thrasher, A. J. (2005). Impaired dendritic-cell homing in vivo in the absence of Wiskott-Aldrich syndrome protein. Blood 105: 1590-1597 [Abstract] [Full Text]  

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