| First Author | Iguchi-Manaka A | Year | 2008 |
| Journal | J Exp Med | Volume | 205 |
| Issue | 13 | Pages | 2959-64 |
| PubMed ID | 19029379 | Mgi Jnum | J:165704 |
| Mgi Id | MGI:4838310 | Doi | 10.1084/jem.20081611 |
| Citation | Iguchi-Manaka A, et al. (2008) Accelerated tumor growth in mice deficient in DNAM-1 receptor. J Exp Med 205(13):2959-64 |
| abstractText | 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. |
