Digoxin and its derivatives suppress Th17 cell differentiation by antagonizing RORγt activity

ABSTRACT: CD4+ T helper lymphocytes that express interleukin-17 (Th17 cells) have critical roles in mouse models of autoimmunity, and there is mounting evidence that they also influence inflammatory processes in humans. Genome-wide association studies in humans have linked genes involved in Th17 cell differentiation and function with susceptibility to Crohn’s disease, rheumatoid arthritis, and psoriasis1-3. Thus, the pathway towards differentiation of Th17 cells and, perhaps, of related innate lymphoid cells with similar effector functions4, 5, is an attractive target for therapeutic applications. Mouse and human Th17 cells are distinguished by expression of the retinoic acid receptor-related orphan nuclear receptor RORγt, which is required for induction of IL-17 transcription and for the manifesta

ORGANISM(S): Mus musculus

SUBMITTER: Jun Huh 

PROVIDER: E-GEOD-27241 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress