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IκBζ regulates TH17 development by cooperating with ROR nuclear receptors

Author

Listed:
  • Kazuo Okamoto

    (Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
    Global Center of Excellence (GCOE) Program, International Research Center for Molecular Science in Tooth and Bone Diseases,
    Japan Science and Technology Agency (JST), ERATO, Takayanagi Osteonetwork Project, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan)

  • 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
    Global Center of Excellence (GCOE) Program, International Research Center for Molecular Science in Tooth and Bone Diseases,)

  • 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
    Global Center of Excellence (GCOE) Program, International Research Center for Molecular Science in Tooth and Bone Diseases,
    Japan Science and Technology Agency (JST), ERATO, Takayanagi Osteonetwork Project, Yushima 1-5-45, Bunkyo-ku, Tokyo 113-8549, Japan)

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.

Suggested Citation

  • Kazuo Okamoto & Yoshiko Iwai & Masatsugu Oh-hora & Masahiro Yamamoto & Tomohiro Morio & Kazuhiro Aoki & Keiichi Ohya & Anton M. Jetten & Shizuo Akira & Tatsushi Muta & Hiroshi Takayanagi, 2010. "IκBζ regulates TH17 development by cooperating with ROR nuclear receptors," Nature, Nature, vol. 464(7293), pages 1381-1385, April.
    • Handle: RePEc:nat:nature:v:464:y:2010:i:7293:d:10.1038_nature08922
    DOI: 10.1038/nature08922
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