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Title: Human Sox4 facilitates the development of CXCL13-producing helper T cells in inflammatory environments
Authors: Yoshitomi, Hiroyuki  kyouindb  KAKEN_id
Kobayashi, Shio
Miyagawa-Hayashino, Aya
Okahata, Akinori
Doi, Kohei
Nishitani, Kohei  kyouindb  KAKEN_id
Murata, Koichi
Ito, Hiromu
Tsuruyama, Tatsuaki  kyouindb  KAKEN_id
Haga, Hironori  kyouindb  KAKEN_id
Matsuda, Shuichi  kyouindb  KAKEN_id
Toguchida, Junya
Author's alias: 吉富, 啓之
小林, 志緒
宮川, 文
西谷, 江平
村田, 浩一
伊藤, 宣
鶴山, 竜昭
羽賀, 博典
松田, 秀一
戸口田, 淳也
Keywords: CD4-positive T cells
Chemokines
Chronic inflammation
Rheumatoid arthritis
Issue Date: 19-Sep-2018
Publisher: Springer Nature America, Inc
Journal title: Nature Communications
Volume: 9
Thesis number: 3762
Abstract: In human inflammatory sites, PD-1hiCXCR5−CD4+ T cells are involved in the formation of ectopic lymphoid-like structures (ELSs) by the secretion of chemokine CXCL13, but how the transcription of CXCL13 is regulated in CD4+ T cells is still unclear. Here we show that Sox4 is a key transcription factor for CXCL13 production in human CD4+ T cells under inflammatory conditions. In vitro TGF-β+, IL-2-neutralizing culture conditions give rise to PD-1hiCXCR5−CD4+ T cells that preferentially express CXCL13, and transcriptome analysis and lentiviral overexpression indicate Sox4 association with the CXCL13 transcription. In vivo, Sox4 is significantly upregulated in synovial CD4+ T cells, when compared with blood CD4+ T cells, from patients with rheumatoid arthritis (RA), and further correlates with ELS formation in RA synovium. Overall, our studies suggest that Sox4 contributes to CXCL13 production and ELS formation at inflammatory sites in humans.
Description: 関節リウマチの病態に関わる転写因子を同定 --炎症環境におけるT細胞の新たな機能解明に期待--. 京都大学プレスリリース. 2018-09-25.
Rights: © The Author(s) 2018. 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.
URI: http://hdl.handle.net/2433/234599
DOI(Published Version): 10.1038/s41467-018-06187-0
PubMed ID: 30232328
Related Link: http://www.kyoto-u.ac.jp/ja/research/research_results/2018/180919_1.html
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