IL-21 initiates an alternative pathway to induce proinflammatory TH17 cells
Thomas Korn,
Estelle Bettelli,
Wenda Gao,
Amit Awasthi,
Anneli Jäger,
Terry B. Strom,
Mohamed Oukka () and
Vijay K. Kuchroo ()
Additional contact information
Thomas Korn: 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
Wenda Gao: Transplant Research Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
Amit Awasthi: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 65 Landsdowne Street, Cambridge, Massachusetts 02139, USA
Anneli Jäger: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Terry B. Strom: Transplant Research Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
Mohamed Oukka: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 65 Landsdowne Street, Cambridge, Massachusetts 02139, USA
Vijay K. Kuchroo: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Nature, 2007, vol. 448, issue 7152, 484-487
Abstract:
TH17 cells are a recently defined subset of pro-inflammatory helper T cells that are induced by the cytokines IL-6 and transforming growth factor (TGF)-β. TH17 can also be induced by an alternative pathway in which TGF-β cooperates with IL-21.
Date: 2007
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DOI: 10.1038/nature05970
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