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Conditional Deletion of TAK1 in T Cells Reveals a Pivotal Role of TCR alpha beta(+) Intraepithelial Lymphocytes in Preventing Lymphopenia-Associated Colitis
http://hdl.handle.net/10091/00021599
http://hdl.handle.net/10091/000215994cdd2e3a-a6d9-4c31-814b-90a292d20fd2
名前 / ファイル | ライセンス | アクション |
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15K08529_01.pdf (7.7 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2019-09-09 | |||||
タイトル | ||||||
タイトル | Conditional Deletion of TAK1 in T Cells Reveals a Pivotal Role of TCR alpha beta(+) Intraepithelial Lymphocytes in Preventing Lymphopenia-Associated Colitis | |||||
言語 | en | |||||
言語 | ||||||
言語 | eng | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1371/journal.pone.0128761 | |||||
関連名称 | 10.1371/journal.pone.0128761 | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Sanjo, Hideki
× Sanjo, Hideki× Tokumaru, Shigeo× Akira, Shizuo× Taki, Shinsuke |
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信州大学研究者総覧へのリンク | ||||||
表示名 | Sanjo, Hideki | |||||
URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.yhTFuNkh.html | |||||
信州大学研究者総覧へのリンク | ||||||
表示名 | Tokumaru, Shigeo | |||||
URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.yUTNbVym.html | |||||
信州大学研究者総覧へのリンク | ||||||
表示名 | Taki, Shinsuke | |||||
URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.OhnFjeyh.html | |||||
出版者 | ||||||
出版者 | PUBLIC LIBRARY SCIENCE | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | PLOS ONE.10(7):e0128761(2015) | |||||
書誌情報 |
PLOS ONE 巻 10, 号 7, p. e0128761, 発行日 2015-07-01 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The kinase TAK is required for the development of conventional and regulatory T cells. We previously reported that mice with conditional deletion of TAK1 in T cells (Lck-cre: TAK1(fl/fl) mice) exhibited severe T lymphopenia, and were nevertheless predisposed to spontaneous colitis with unknown etiology. Here we focused on the immunopathological mechanism in colitic Lck-cre: TAK1(fl/fl) mice. We found that 'leaky' CD4(+) T cells retaining TAK1 acquired inflammatory phenotypes that contribute to disease onset in Lck-cre: TAK1(fl/fl) mice. Furthermore, the gut microbiota-triggered signaling was also a key event leading to the pathogenesis. We discovered that Lck-cre: TAK1(fl/fl) mice were almost completely devoid of TCR alpha beta(+) CD8 alpha(+) intestinal intraepithelial lymphocytes (IELs) and this was largely due to the developmental defect of the thymic precursors by TAK1 deficiency. Remarkably, transfer of TCR alpha beta(+) CD8 alpha(+) IELs from wild-type mice ameliorated colitis in Lck-cre: TAK1(fl/fl) mice. Taken together, our current study highlighted the emerging role of TAK1 in configuring the gut-specialized T cell subset, which regulates mucosal homeostasis under lymphopenic conditions. | |||||
資源タイプ(コンテンツの種類) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Article | |||||
ISSN | ||||||
収録物識別子タイプ | EISSN | |||||
収録物識別子 | 1932-6203 | |||||
PubMed | ||||||
識別子タイプ | PMID | |||||
関連識別子 | https://www.ncbi.nlm.nih.gov/pubmed/26132627 | |||||
関連名称 | 26132627 | |||||
権利 | ||||||
権利情報 | © 2015 Sanjo 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 | |||||
出版タイプ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
WoS | ||||||
表示名 | Web of Science | |||||
URL | http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000358153000019 |