IκBζ regulates TH17 development by cooperating with ROR nuclear receptors

Kazuo Okamoto, Yoshiko Iwai, Masatsugu Oh-hora, Masahiro Yamamoto, Tomohiro Morio, Kazuhiro Aoki, Keiichi Ohya, Anton M. Jetten, Shizuo Akira, Tatsushi Muta and Hiroshi Takayanagi ()
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Kazuo Okamoto: Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
Yoshiko Iwai: Medical Top Track Program, Medical Research Institute, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8510, Japan
Masatsugu Oh-hora: Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
Masahiro Yamamoto: Laboratory of Immune Regulation, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University, 2-2, Yamada-oka, Suita, Osaka 565-0871, Japan
Tomohiro Morio: Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8519, Japan
Kazuhiro Aoki: Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan
Keiichi Ohya: Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan
Anton M. Jetten: Cell Biology Section, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T.W. Alexander Drive Research Triangle Park, North Carolina 27709, USA
Shizuo Akira: Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, Yamada-oka 3-1, Suita, Osaka 565-0871, Japan
Tatsushi Muta: Laboratory of Cell Recognition and Response, Graduate School of Life Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan
Hiroshi Takayanagi: Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University

Nature, 2010, vol. 464, issue 7293, 1381-1385

Abstract: IκBζ and TH17 cell development The development of interleukin (IL)-17-producing T cells (TH17 cells) is shown to require the transcription factor IκBζ in addition to ROR nuclear receptors. IκBζ cooperates with ROR factors through binding to the upstream conserved non-coding sequence CNS2, and mice deficient for IκBζ are resistant to the induction of experimental autoimmune encephalomyelitis. The work highlights the transcriptional mechanisms involved in TH17 development and suggests novel therapeutic approaches to autoimmune disease.

Date: 2010
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DOI: 10.1038/nature08922

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