期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 205, 期 13, 页码 2959-2964出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20081611
关键词
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资金
- Ministry of Education, Science and Culture of Japan
- Program for Promotion of Fundamental Studies in Health Science of the National Institute of Biomedical Innovation (NIBIO)
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.
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