Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1

Chuan Wu, Nir Yosef, Theresa Thalhamer, Chen Zhu, Sheng Xiao, Yasuhiro Kishi, Aviv Regev () and Vijay K. Kuchroo ()
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Chuan Wu: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Nir Yosef: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Theresa Thalhamer: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Chen Zhu: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Sheng Xiao: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Yasuhiro Kishi: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Aviv Regev: Broad Institute of MIT and Harvard, 7 Cambridge Center
Vijay K. Kuchroo: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School

Nature, 2013, vol. 496, issue 7446, 513-517

Abstract: Transcriptional profiling of developing TH17 cells identifies serum glucocorticoid kinase 1 (SGK1) as an essential node downstream of IL-23 signalling, and transcriptional analysis shows that a modest increase in salt concentration induces SGK1 expression, promotes IL-23 receptor expression and enhances TH17 cell differentiation, accelerating the development of autoimmunity.

Date: 2013
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DOI: 10.1038/nature11984

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