Journal
CELL REPORTS
Volume 22, Issue 3, Pages 653-665Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.12.068
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Funding
- National Multiple Sclerosis Society (Career Transition Award) [TA 3059-A-2]
- US NIH (R00 NIH Pathway to Independence Award) [R00AI110649A, K01DK090105, P01AI073748, P01AI056299, P01AI039671, R01NS045937, R01 NS030843]
- Austrian Science Fund (FWF) [J3091-B12]
- NATIONAL CANCER INSTITUTE [ZIABC011801] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R00AI110649, P01AI056299, P01AI039671, P01AI073748] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K01DK090105] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS045937, R01NS030843] Funding Source: NIH RePORTER
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A balance between Th17 and regulatory T (Treg) cells is critical for immune homeostasis and tolerance. Our previous work has shown Serum-and glucocorticoid- induced kinase 1 (SGK1) is critical for the development and function of Th17 cells. Here, we show that SGK1 restrains the function of Treg cells and reciprocally regulates development of Th17/Treg balance. SGK1 deficiency leads to protection against autoimmunity and enhances self-tolerance by promoting Treg cell development and disarming Th17 cells. Treg cell-specific deletion of SGK1 results in enhanced Treg cell-suppressive function through preventing Foxo1 out of the nucleus, thereby promoting Foxp3 expression by binding to Foxp3 CNS1 region. Furthermore, our data suggest that SGK1 also plays a critical role in IL-23R-mediated inhibition of Treg and development of Th17 cells. Therefore, we demonstrate that SGK1 functions as a pivotal node in regulating the reciprocal development of pro-inflammatory Th17 and Foxp3 + Treg cells during autoimmune tissue inflammation.
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