Title: Systematic analysis of Th17 network reveals novel IL-23 signaling circuits

Presenter: Dr. WU Chuan

University: Brigham and Women’s Hospital, Harvard Medical School

Time: 10:00-11:00, December 6, 2012

Venue: Room A203, Institute of Microbiology, Chinese Academy of Sciences

Abstract: We used unbiased transcriptional profiling of developing Th17 cells to construct a model of their signaling network and identify major nodes that regulate Th17 development. We identified serum glucocorticoid kinase-1 (SGK1), as an essential node downstream of IL-23 signaling, critical for regulating IL-23R expression and for stabilizing Th17 cell phenotype. In addition, we revealed high salt levels induce differentiation of pathogenic Th17 cells and impair the differentiation and/or function of Tregs in vitro and in vivo, thereby promoting induction of autoimmunity.