Foxo1 Drives the TGFβ1-Dependent Dichotomy of Th17 Cell Fates
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1023848 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26277064_1.fastq.gz | Fastqsanger.gz | |||
| SRR26277064_2.fastq.gz | Fastqsanger.gz | |||
| SRR26277065_1.fastq.gz | Fastqsanger.gz | |||
| SRR26277065_2.fastq.gz | Fastqsanger.gz |
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Project description:Th17 cells are key players in autoimmune diseases. However, the roles of non-coding RNAs in Th17 cells are largely unknown. Here, we show that deletion of the Dicer gene specifically in Th17 cells protects from experimental autoimmune encephalomyelitis (EAE). Th17 cells highly express the miR-183/96/182 cluster (miR-183C), in response to IL-6/STAT3 signaling. Moreover, miR-183C regulates pathogenic cytokine expression during Th17 development. Furthermore, transcription factor Foxo1 is one of functional targets of miR-183C in Th17 cells: Foxo1 negatively regulates the pathogenicity of Th17 cells and miR-183C represses Foxo1 expression. Collectively, our results demonstrate one of crucial roles for miR-183C cluster in regulation of Th17 cell function in autoimmune diseases.
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