The Journal of Experimental Medicine
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Published online November 24, 2008
doi:10.1084/jem.20081611
The Journal of Experimental Medicine, Vol. 205, No. 13, 2959-2964
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Iguchi-Manaka et al.
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BRIEF DEFINITIVE REPORT

 Accelerated tumor growth in mice deficient in DNAM-1 receptor

Akiko Iguchi-Manaka1, Hirayasu Kai1, Yumi Yamashita1, Kai Shibata1, Satoko Tahara-Hanaoka1, Shin-ichiro Honda1, Teruhito Yasui2, Hitoshi Kikutani2, Kazuko Shibuya1, and Akira Shibuya1

1 Department of Immunology, Institute of Basic Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki 305-8575, Japan
2 Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan

CORRESPONDENCE Akira Shibuya: ashibuya{at}md.tsukuba.ac.jp OR Kazuko Shibuya: kazukos{at}md.tsukuba.ac.jp

Since the identification of ligands for human and mouse DNAM-1, emerging evidence has suggested that DNAM-1 plays an important role in the T cell– and natural killer (NK) cell–mediated recognition and lysis of tumor cells. However, it remains undetermined whether DNAM-1 is involved in tumor immune surveillance in vivo. We addressed this question by using DNAM-1–deficient mice. DNAM-1–deficient cytotoxic T lymphocyte (CTL) and NK cells showed significantly less cytotoxic activity against DNAM-1 ligand-expressing tumors in vitro than wild-type (WT) cells. The methylcholanthrene (MCA)-induced fibrosarcoma cell line Meth A expressed the DNAM-1 ligand CD155, and DNAM-1–deficient mice showed increased tumor development and mortality after transplantation of Meth A cells. Moreover, the DNAM-1–deficient mice developed significantly more DNAM-1 ligand-expressing fibrosarcoma and papilloma cells in response to the chemical carcinogens MCA and 7,12-dimethylbenz[a]anthracene (DMBA), respectively, than did WT mice. These results indicate that DNAM-1 plays an important role in immune surveillance of tumor development.

A. Iguchi-Manaka and H. Kai contributed equally to this paper.

© 2008 Iguchi-Manaka et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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