Induction of pathogenic Th17 cells by salt inducible kinase SGK-1 (NaCl)

ABSTRACT: Th17 cells are highly proinflammatory cells that are critical for clearing extracellular pathogens like fungal infections and for induction of multiple autoimmune diseases1. IL-23 plays a critical role in stabilizing and endowing Th17 cells with pathogenic effector functions2. Previous studies have shown that IL-23 signaling reinforces the Th17 phenotype by increasing expression of IL-23 receptor (IL-23R)3. However, the precise molecular mechanism by which IL-23 sustains the Th17 response and induces pathogenic effector functions has not been elucidated. Here, 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 es

ORGANISM(S): Mus musculus

SUBMITTER: Nir Yosef 

PROVIDER: E-GEOD-43957 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress