ダウンロード数: 403
このアイテムのファイル:
ファイル | 記述 | サイズ | フォーマット | |
---|---|---|---|---|
journal.ppat.1001274.pdf | 4.04 MB | Adobe PDF | 見る/開く |
タイトル: | HTLV-1 bZIP Factor Induces T-Cell Lymphoma and Systemic Inflammation In Vivo |
著者: | Satou, Yorifumi Yasunaga, Jun-ichirou ![]() Zhao, Tiejun Yoshida, Mika Miyazato, Paola Takai, Ken Shimizu, Kei Ohshima, Koichi Green, Patrick L. Ohkura, Naganari Yamaguchi, Tomoyuki Ono, Masahiro Sakaguchi, Shimon Matsuoka, Masao ![]() |
著者名の別形: | 松岡, 雅雄 |
発行日: | 10-Feb-2011 |
出版者: | Public Library of Science |
誌名: | PLoS Pathogens |
巻: | 7 |
号: | 2 |
論文番号: | e1001274 |
抄録: | Human T-cell leukemia virus type 1 (HTLV-1) is the causal agent of a neoplastic disease of CD4+ T cells, adult T-cell leukemia (ATL), and inflammatory diseases including HTLV-1 associated myelopathy/tropical spastic paraparesis, dermatitis, and inflammatory lung diseases. ATL cells, which constitutively express CD25, resemble CD25+CD4+ regulatory T cells (Treg). Approximately 60% of ATL cases indeed harbor leukemic cells that express FoxP3, a key transcription factor for Treg cells. HTLV-1 encodes an antisense transcript, HTLV-1 bZIP factor (HBZ), which is expressed in all ATL cases. In this study, we show that transgenic expression of HBZ in CD4+ T cells induced T-cell lymphomas and systemic inflammation in mice, resembling diseases observed in HTLV-1 infected individuals. In HBZ-transgenic mice, CD4+Foxp3+ Treg cells and effector/memory CD4+ T cells increased in vivo. As a mechanism of increased Treg cells, HBZ expression directly induced Foxp3 gene transcription in T cells. The increased CD4+Foxp3+ Treg cells in HBZ transgenic mice were functionally impaired while their proliferation was enhanced. HBZ could physically interact with Foxp3 and NFAT, thereby impairing the suppressive function of Treg cells. Thus, the expression of HBZ in CD4+ T cells is a key mechanism of HTLV-1-induced neoplastic and inflammatory diseases. |
記述: | HTLV-1 bZIP factorは発がんと炎症を起こす. 京都大学プレスリリース. 2011-02-11. |
著作権等: | © 2011 Satou et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
URI: | http://hdl.handle.net/2433/137213 |
DOI(出版社版): | 10.1371/journal.ppat.1001274 |
PubMed ID: | 21347344 |
関連リンク: | http://www.kyoto-u.ac.jp/ja/news_data/h/h1/news6/2010/110211_1.htm |
出現コレクション: | 学術雑誌掲載論文等 |
![](/dspace/image/articlelinker.gif)
このリポジトリに保管されているアイテムはすべて著作権により保護されています。