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| ファイル | 記述 | サイズ | フォーマット | |
|---|---|---|---|---|
| s12977-020-0511-0.pdf | 785.67 kB | Adobe PDF | 見る/開く |
| タイトル: | HTLV-1 bZIP factor: the key viral gene for pathogenesis |
| 著者: | Matsuoka, Masao Mesnard, Jean-Michel |
| 著者名の別形: | 松岡, 雅雄 |
| 発行日: | 8-Jan-2020 |
| 出版者: | Springer Nature |
| 誌名: | Retrovirology |
| 巻: | 17 |
| 論文番号: | 2 |
| 抄録: | Human T cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases. The HTLV-1 bZIP factor (HBZ) gene is constantly expressed in HTLV-1 infected cells and ATL cells. HBZ protein suppresses transcription of the tax gene through blocking the LTR recruitment of not only ATF/CREB factors but also CBP/p300. HBZ promotes transcription of Foxp3, CCR4, and T-cell immunoreceptor with Ig and ITIM domains (TIGIT). Thus, HBZ is critical for the immunophenotype of infected cells and ATL cells. HBZ also functions in its RNA form. HBZ RNA suppresses apoptosis and promotes proliferation of T cells. Since HBZ RNA is not recognized by cytotoxic T cells, HTLV-1 has a clever strategy for avoiding immune detection. HBZ plays central roles in maintaining infected T cells in vivo and determining their immunophenotype. |
| 著作権等: | © The Author(s) 2020. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
| URI: | http://hdl.handle.net/2433/245699 |
| DOI(出版社版): | 10.1186/s12977-020-0511-0 |
| PubMed ID: | 31915026 |
| 出現コレクション: | 学術雑誌掲載論文等 |
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