MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting IL-23 responsiveness and effector gene expression
Ontology highlight
ABSTRACT: We examined the role of miR-155 in differentiated Th17 cells during their induction of Experimental Autoimmune Encephalomyelitis (EAE). Using adoptive transfer experiments, we found that highly purified, MOG antigen specific Th17 cells lacking miR-155 are defective in their capacity to cause EAE. Gene expression profiling of purified miR-155-/- IL-17F+ Th17 cells identified a subset of effector genes that are dependent upon miR-155 for their proper expression through a mechanism involving repression of the transcription factor Ets1. Among the genes reduced in the absence of miR-155 was IL-23R, resulting in miR-155-/- Th17 cells being hypo-responsive to IL-23. Taken together, our study demonstrates a critical role for miR-155 in Th17 cells as they unleash autoimmune inflammation, and finds that this occurs through a signaling network involving miR-155, Ets1 and the clinically relevant IL-23-IL-23R pathway.
ORGANISM(S): Mus musculus
PROVIDER: GSE45122 | GEO | 2013/05/01
SECONDARY ACCESSION(S): PRJNA192933
REPOSITORIES: GEO
ACCESS DATA