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Accelerated tumor growth in mice deficient in DNAM-1 receptor
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 s...
Autores principales: | , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605241/ https://www.ncbi.nlm.nih.gov/pubmed/19029379 http://dx.doi.org/10.1084/jem.20081611 |
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author | Iguchi-Manaka, Akiko Kai, Hirayasu Yamashita, Yumi Shibata, Kai Tahara-Hanaoka, Satoko Honda, Shin-ichiro Yasui, Teruhito Kikutani, Hitoshi Shibuya, Kazuko Shibuya, Akira |
author_facet | Iguchi-Manaka, Akiko Kai, Hirayasu Yamashita, Yumi Shibata, Kai Tahara-Hanaoka, Satoko Honda, Shin-ichiro Yasui, Teruhito Kikutani, Hitoshi Shibuya, Kazuko Shibuya, Akira |
author_sort | Iguchi-Manaka, Akiko |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2605241 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-26052412009-06-22 Accelerated tumor growth in mice deficient in DNAM-1 receptor Iguchi-Manaka, Akiko Kai, Hirayasu Yamashita, Yumi Shibata, Kai Tahara-Hanaoka, Satoko Honda, Shin-ichiro Yasui, Teruhito Kikutani, Hitoshi Shibuya, Kazuko Shibuya, Akira J Exp Med Brief Definitive Reports 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. The Rockefeller University Press 2008-12-22 /pmc/articles/PMC2605241/ /pubmed/19029379 http://dx.doi.org/10.1084/jem.20081611 Text en © 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/). |
spellingShingle | Brief Definitive Reports Iguchi-Manaka, Akiko Kai, Hirayasu Yamashita, Yumi Shibata, Kai Tahara-Hanaoka, Satoko Honda, Shin-ichiro Yasui, Teruhito Kikutani, Hitoshi Shibuya, Kazuko Shibuya, Akira Accelerated tumor growth in mice deficient in DNAM-1 receptor |
title | Accelerated tumor growth in mice deficient in DNAM-1 receptor |
title_full | Accelerated tumor growth in mice deficient in DNAM-1 receptor |
title_fullStr | Accelerated tumor growth in mice deficient in DNAM-1 receptor |
title_full_unstemmed | Accelerated tumor growth in mice deficient in DNAM-1 receptor |
title_short | Accelerated tumor growth in mice deficient in DNAM-1 receptor |
title_sort | accelerated tumor growth in mice deficient in dnam-1 receptor |
topic | Brief Definitive Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605241/ https://www.ncbi.nlm.nih.gov/pubmed/19029379 http://dx.doi.org/10.1084/jem.20081611 |
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