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Blood, 1 August 2005, Vol. 106, No. 3, pp. 779-786. Prepublished online as a Blood First Edition Paper on April 5, 2005; DOI 10.1182/blood-2005-02-0817. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-02-0817v1 106/3/779    most recent Alert me when this article is cited Alert me if a correction is posted 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 Boles, K. S Articles by Colonna, M. Search for Related Content PubMed PubMed Citation Articles by Boles, K. S Articles by Colonna, M. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 28, 2005 Accepted March 30, 2005 The tumor suppressor TSLC1/NECL-2 triggers NK cell and CD8+ T cell responses through the cell surface receptor CRTAM Kent S Boles, Winfried Barchet, Tom Diacovo, Marina Cella, and Marco Colonna* Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA Department of Pediatrics, Washington University School of Medicine, St Louis, MO, USA * Corresponding author; email: mcolonna{at}pathology.wustl.edu. The tumor suppressor in lung cancer-1 (TSLC1) gene is frequently silenced in human lung carcinomas and its expression suppresses tumorigenesis in nude mice. TSLC1 encodes a cell surface protein called Necl-2 that belongs to the Nectin and Nectin-like (Necl) family of molecules. Necl-2 mediates epithelial cell junctions by homotypic contacts and/or heterotypic interactions with other Nectins and Necls. Thus, it inhibits tumorigenesis by ensuring that epithelial cells grow in organized layers. Here we demonstrate that NK cells and CD8+ T cells recognize Necl-2 through a receptor known as class I-restricted T cell-associated molecule (CRTAM), which is expressed only on activated cells. CRTAM-Necl-2 interactions promote cytotoxicity of NK cells and IFN- secretion of CD8+ T cells in vitro as well as NK cell-mediated rejection of tumors expressing Necl-2 in vivo. These results provide evidence for an additional mechanism of tumor suppression mediated by TSLC1 that involves cytotoxic lymphocytes. Furthermore, they reveal Necl-2 as one of the molecular targets that allows the immunosurveillance network to distinguish tumor cells from normal cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Immune surveillance against common cancers: the great escape Michael A. Caligiuri Blood 2005 106: 773-774. [Full Text] [PDF] This article has been cited by other articles: P. Maurel, S. Einheber, J. Galinska, P. Thaker, I. Lam, M. B. Rubin, S. S. Scherer, Y. Murakami, D. H. Gutmann, and J. L. Salzer Nectin-like proteins mediate axon Schwann cell interactions along the internode and are essential for myelination J. Cell Biol., August 27, 2007; 178(5): 861 - 874. [Abstract] [Full Text] [PDF] S. Schwartzkopff, C. Grundemann, O. Schweier, S. Rosshart, K. E. Karjalainen, K.-F. Becker, and H. Pircher Tumor-Associated E-Cadherin Mutations Affect Binding to the Killer Cell Lectin-Like Receptor G1 in Humans J. Immunol., July 15, 2007; 179(2): 1022 - 1029. [Abstract] [Full Text] [PDF] H. L. Lung, A. K. Leung Cheung, D. Xie, Y. Cheng, F. M. Kwong, Y. Murakami, X.-Y. Guan, J. S. Sham, D. Chua, A. I. Protopopov, et al. TSLC1 Is a Tumor Suppressor Gene Associated with Metastasis in Nasopharyngeal Carcinoma Cancer Res., October 1, 2006; 66(19): 9385 - 9392. [Abstract] [Full Text] [PDF] S. A. Cormier, A. G. Taranova, C. Bedient, T. Nguyen, C. Protheroe, R. Pero, D. Dimina, S. I. Ochkur, K. O'Neill, D. Colbert, et al. Pivotal Advance: Eosinophil infiltration of solid tumors is an early and persistent inflammatory host response J. Leukoc. Biol., June 1, 2006; 79(6): 1131 - 1139. [Abstract] [Full Text] [PDF] L. van der Weyden, M. J. Arends, O. E. Chausiaux, P. J. Ellis, U. C. Lange, M. A. Surani, N. Affara, Y. Murakami, D. J. Adams, and A. Bradley Loss of TSLC1 Causes Male Infertility Due to a Defect at the Spermatid Stage of Spermatogenesis. Mol. Cell. Biol., May 1, 2006; 26(9): 3595 - 3609. [Abstract] [Full Text] [PDF] M. Colonna Cytolytic responses: cadherins put out the fire J. Exp. Med., February 20, 2006; 203(2): 261 - 264. [Abstract] [Full Text] [PDF]

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