| First Author | Wu C | Year | 2018 |
| Journal | Cell Rep | Volume | 22 |
| Issue | 3 | Pages | 653-665 |
| PubMed ID | 29346764 | Mgi Jnum | J:270790 |
| Mgi Id | MGI:6278726 | Doi | 10.1016/j.celrep.2017.12.068 |
| Citation | Wu C, et al. (2018) SGK1 Governs the Reciprocal Development of Th17 and Regulatory T Cells. Cell Rep 22(3):653-665 |
| abstractText | 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. |
