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Suppression of TH17 differentiation and autoimmunity by a synthetic ROR ligand

Author

Listed:
  • Laura A. Solt

    (The Scripps Research Institute)

  • Naresh Kumar

    (The Scripps Research Institute
    The Scripps Research Institute Molecular Screening Center, The Scripps Research Institute)

  • Philippe Nuhant

    (The Scripps Research Institute)

  • Yongjun Wang

    (The Scripps Research Institute)

  • Janelle L. Lauer

    (The Scripps Research Institute)

  • Jin Liu

    (The Scripps Research Institute)

  • Monica A. Istrate

    (The Scripps Research Institute
    The Scripps Research Institute Molecular Screening Center, The Scripps Research Institute)

  • Theodore M. Kamenecka

    (The Translational Research Institute, The Scripps Research Institute)

  • William R. Roush

    (The Scripps Research Institute)

  • Dušica Vidović

    (The Scripps Research Institute Molecular Screening Center, The Scripps Research Institute
    Center for Computational Science University of Miami)

  • Stephan C. Schürer

    (The Scripps Research Institute Molecular Screening Center, The Scripps Research Institute
    Center for Computational Science University of Miami)

  • Jihong Xu

    (University of Arkansas for Medical Sciences)

  • Gail Wagoner

    (University of Arkansas for Medical Sciences)

  • Paul D. Drew

    (University of Arkansas for Medical Sciences)

  • Patrick R. Griffin

    (The Scripps Research Institute
    The Scripps Research Institute Molecular Screening Center, The Scripps Research Institute
    The Translational Research Institute, The Scripps Research Institute)

  • Thomas P. Burris

    (The Scripps Research Institute)

Abstract

A new class of immunomodulator The nuclear receptors RORα and RORγt (retinoic acid receptor-related orphan receptors α and γt) are essential for the development of TH17 cells, the T-helper cells that produce interleukin-17. Two groups report the identification of RORγt inhibitors, compounds that could have potential in the treatment of autoimmune diseases. Huh et al. used a chemical screen in an insect-cell-based reporter system to identify the cardiac glycoside digoxin and various derivatives as inhibitors of the transcriptional activity of RORγt. Through this mechanism, these compounds block the differentiation of TH17 cells in mice, and inhibit interleukin-17 production in vitro in human T cells. Solt et al. describe a synthetic ligand, named SR1001, that functions as an inverse agonist for RORα and RORγt, and show that it blocks TH17 development in vitro and inhibits experimental encephalomyelitis in mice.

Suggested Citation

  • Laura A. Solt & Naresh Kumar & Philippe Nuhant & Yongjun Wang & Janelle L. Lauer & Jin Liu & Monica A. Istrate & Theodore M. Kamenecka & William R. Roush & Dušica Vidović & Stephan C. Schürer & Jihong, 2011. "Suppression of TH17 differentiation and autoimmunity by a synthetic ROR ligand," Nature, Nature, vol. 472(7344), pages 491-494, April.
    • Handle: RePEc:nat:nature:v:472:y:2011:i:7344:d:10.1038_nature10075
    DOI: 10.1038/nature10075
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    Cited by:

    1. Meghan H. Murray & Aurore Cecile Valfort & Thomas Koelblen & Céline Ronin & Fabrice Ciesielski & Arindam Chatterjee & Giri Babu Veerakanellore & Bahaa Elgendy & John K. Walker & Lamees Hegazy & Thomas, 2022. "Structural basis of synthetic agonist activation of the nuclear receptor REV-ERB," Nature Communications, Nature, vol. 13(1), pages 1-12, December.

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