Th17 cell regulation: The link to salt-sensing and SGK1 Th17 cell phenotype induction

This presentation was given by Chuan We from Brigham and Women’s Hospital, Harvard Medical School, USA. It was presented at the ISN’s Forefronts Symposium 2015 taking place in Shenzhen, China, on October 22-25, 2015 for which the theme was ‘Immunomodulation of Cardio-Renal Function’ during Session 7: Novel Mechanisms in Salt and Water Homeostasis.


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 Presentation Abstract: 

Interleukin-23 (IL-23) and its receptor IL-23 receptor (IL-23R) are involved in regulating the pathogenicity of Th17 cells. IL-23R expression has been shown to be associated with inflammatory autoimmune disease. However, the downstream pathways of IL-23R signaling have not been fully elucidated. Here we demonstrate that serum glucocorticoid kinase-1 (SGK1) is one of the critical downstream elements for IL-23 signaling, maintaining the Th17 phenotype and IL-23R expression in the intestinal inflammation. In a T cell induced-colitis model, SGK1 promoted inflammatory Th17 cells in the intestine and inhibited the development of the Foxp3+ Treg cells during disease. We showed here for the first time that SGK1 plays a crucial role in the regulation of IL-23R expression and Th17 cell maintenance. Meanwhile, considering SGK1 directing the reciprocal differentiation of Teff and Treg cells, we also illustrate Foxp3 plays the dominant role to overcome SGK1 regulating Teff cell differentiation.

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