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| ファイル | 記述 | サイズ | フォーマット | |
|---|---|---|---|---|
| srep42888.pdf | 1.93 MB | Adobe PDF | 見る/開く |
| タイトル: | Cbx3/HP1γ deficiency confers enhanced tumor-killing capacity on CD8+ T cells |
| 著者: | Sun, Michael Ha, Ngoc Pham, Duc-Hung Frederick, Megan Sharma, Bandana Naruse, Chie   Asano, Masahide Pipkin, Matthew E. George, Rani E. Thai, To-Ha |
| 著者名の別形: | 浅野, 雅秀 |
| 発行日: | 21-Feb-2017 |
| 出版者: | Springer Nature |
| 誌名: | Scientific Reports |
| 巻: | 7 |
| 論文番号: | 42888 |
| 記述: | Cbx3/HP1γ is a histone reader whose function in the immune system is not completely understood. Here, we demonstrate that in CD8+ T cells, Cbx3/HP1γ insufficiency leads to chromatin remodeling accompanied by enhanced Prf1, Gzmb and Ifng expression. In tumors obtained from Cbx3/HP1γ- insufficient mice or wild type mice treated with Cbx3/HP1γ-insufficient CD8+ T cells, there is an increase of CD8+ effector T cells expressing the stimulatory receptor Klrk1/NKG2D, a decrease in CD4+ CD25+ FOXP3+ regulatory T cells (Treg cells) as well as CD25+ CD4+ T cells expressing the inhibitory receptor CTLA4. Together these changes in the tumor immune environment may have mitigated tumor burden in Cbx3/HP1γ-insufficient mice or wild type mice treated with Cbx3/HP1γ-insufficient CD8+ T cells. These findings suggest that targeting Cbx3/HP1γ can represent a rational therapeutic approach to control growth of solid tumors. |
| 著作権等: | This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
| URI: | http://hdl.handle.net/2433/218632 |
| DOI(出版社版): | 10.1038/srep42888 |
| PubMed ID: | 28220815 |
| 出現コレクション: | 学術雑誌掲載論文等 |
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