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IL-21 and TGF-β are required for differentiation of human TH17 cells

Author

Listed:
  • Li Yang

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

  • David E. Anderson

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Clare Baecher-Allan

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

  • William D. Hastings

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Estelle Bettelli

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Mohamed Oukka

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

  • Vijay K. Kuchroo

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

  • David A. Hafler

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA)

Abstract

Cytokines involved in TH17 cell differentiation TH17 cells (a subset of interleukin (IL)-17-producing T helper cells) are thought to contribute to the pathogenesis of a number of human autoimmune diseases. This study examines which cytokines are required for the production of IL-17A by memory and naive human CD4 T cells. The data demonstrate that transforming growth factor-β (TGF-β) is critical for the differentiation of TH17 cells from highly purified naive CD4+ T cells, but not necessary for induction of IL-17 from committed memory CD4+ T cells.

Suggested Citation

  • Li Yang & David E. Anderson & Clare Baecher-Allan & William D. Hastings & Estelle Bettelli & Mohamed Oukka & Vijay K. Kuchroo & David A. Hafler, 2008. "IL-21 and TGF-β are required for differentiation of human TH17 cells," Nature, Nature, vol. 454(7202), pages 350-352, July.
  • Handle: RePEc:nat:nature:v:454:y:2008:i:7202:d:10.1038_nature07021
    DOI: 10.1038/nature07021
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