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  1. 学術雑誌論文
  2. その他
  1. 部局別インデックス
  2. 医学部

IL-10-mediated signals act as a switch for lymphoproliferation in Human T-cell leukemia virus type-1 infection by activating the STAT3 and IRF4 pathways

http://hdl.handle.net/20.500.12000/45640
http://hdl.handle.net/20.500.12000/45640
7519f943-c1ae-4169-a1b8-0b32cc38caa4
名前 / ファイル ライセンス アクション
journal.ppat.1006597.pdf journal.ppat.1006597.pdf
Item type デフォルトアイテムタイプ(フル)(1)
公開日 2020-04-15
タイトル
タイトル IL-10-mediated signals act as a switch for lymphoproliferation in Human T-cell leukemia virus type-1 infection by activating the STAT3 and IRF4 pathways
言語 en
作成者 Sawada, Leila

× Sawada, Leila

en Sawada, Leila

Nagano, Yoshiko

× Nagano, Yoshiko

en Nagano, Yoshiko

Hasegawa, Atsuhiko

× Hasegawa, Atsuhiko

en Hasegawa, Atsuhiko

Kenai, Hikari

× Kenai, Hikari

en Kenai, Hikari

Nogami, Kai

× Nogami, Kai

en Nogami, Kai

Ito, Sayaka

× Ito, Sayaka

en Ito, Sayaka

Sato, Tomoo

× Sato, Tomoo

en Sato, Tomoo

Yamano, Yoshihisa

× Yamano, Yoshihisa

en Yamano, Yoshihisa

Tanaka, Yuetsu

× Tanaka, Yuetsu

en Tanaka, Yuetsu

Masuda, Takao

× Masuda, Takao

en Masuda, Takao

Kannagi, Mari

× Kannagi, Mari

en Kannagi, Mari

アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
言語 en
権利情報 Creative Commons Attribution License 4.0
言語 en
権利情報Resource https://creativecommons.org/licenses/by/4.0/
権利情報 https://creativecommons.org/licenses/by/4.0/
内容記述
内容記述タイプ Other
内容記述 Human T-cell leukemia virus type-1 (HTLV-1) causes two distinct diseases, adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Since there are no disease-specific differences among HTLV-1 strains, the etiological mechanisms separating these respective lymphoproliferative and inflammatory diseases are not well understood. In this study, by using IL-2-dependent HTLV-1-infected Tcell lines (ILTs) established from patients with ATL and HAM/TSP, we demonstrate that the anti-inflammatory cytokine IL-10 and its downstream signals potentially act as a switch for proliferation in HTLV-1-infected cells. Among six ILTs used, ILTs derived from all three ATL patients grew much faster than those from three HAM/TSP patients. Although most of the ILTs tested produced IFN-γ and IL-6, the production of IL-10 was preferentially observed in the rapid-growing ILTs. Interestingly, treatment with exogenous IL-10 markedly enhanced proliferation of the slow-growing HAM/TSP-derived ILTs. The IL-10-mediated proliferation of these ILTs was associated with phosphorylation of STAT3 and induction of survivin and IRF4, all of which are characteristics of ATL cells. Knockdown of STAT3 reduced expression of IL-10, implying a positive-feedback regulation between STAT3 and IL-10. STAT3 knockdown also reduced survivin and IRF4 in the IL-10- producing or IL-10- treated ILTs. IRF4 knockdown further suppressed survivin expression and the cell growth in these ILTs. These findings indicate that the IL-10-mediated signals promote cell proliferation in HTLV-1- infected cells through the STAT3 and IRF4 pathways. Our results imply that, although HTLV-1 infection alone may not be sufficient for cell proliferation, IL-10 and its signaling pathways within the infected cell itself and/or its surrounding microenvironment may play a critical role in pushing HTLV-1-infected cells towards proliferation at the early stages of HTLV-1 leukemogenesis. This study provides useful information for understanding of disease mechanisms and disease-prophylactic strategies in HTLV-1 infection.
内容記述タイプ Other
内容記述 論文
出版者
言語 en
出版者 Public Library of Science
言語
言語 eng
資源タイプ
資源タイプ journal article
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
識別子
識別子 http://hdl.handle.net/20.500.12000/45640
識別子タイプ HDL
関連情報
関連識別子
識別子タイプ DOI
関連識別子 https://doi.org/10.1371/journal.ppat.1006597
関連識別子
識別子タイプ DOI
関連識別子 https://doi.org/10.1371/journal.ppat.1006597
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1553-7374
収録物名
言語 en
収録物名 PLOS Pathogens
書誌情報
巻 13, 号 9
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