Genomics

Dataset Information

245

Genome-wide binding of STAT3 and STAT5 under Th17 conditions (ChIP-Seq)


ABSTRACT: Interleukin 2 (IL-2), a cytokine linked to human autoimmune diseases, limits IL-17 production. We show that deletion of Stat3 in T cells abrogates IL-17 production and attenuates autoimmunity associated with IL-2 deficiency. While STAT3 induces IL-17 and RORγt and inhibits Foxp3, IL-2 inhibited IL-17 independently of Foxp3 and RORγt. We found that STAT3 and STAT5 bound to multiple common sites across the Il17 genetic locus. The induction of STAT5 binding by IL-2 was associated with a reduction in STAT3 binding at these sites and the inhibition of associated active epigenetic marks. Titrating the relative activation of STAT3 and STAT5 modulated TH17 cell specification. Thus, the balance rather than the absolute magnitude of these signals determines the propensity of cells to make a key inflammatory cytokine. The genome-wide binding of STAT3 and STAT5 under Th17 conditions was investigated by CHIP-seq.

ORGANISM(S): Mus musculus  

SUBMITTER: Scott M Steward-Tharp   Hong-Wei Sun  Arian Laurence  Kamran Ghoreschi  Kiyoshi Hirahara  Xiang-Ping Yang  Jinfang Zhu  Jaime Rodriguez-Canales  John R Grainger  John J O’Shea  Lai Wei  Yuka Kanno  Golnaz Vahedi 

PROVIDER: E-GEOD-26552 | ArrayExpress | 2011-02-09

SECONDARY ACCESSION(S): GSE26552SRP005277PRJNA142287

REPOSITORIES: GEO, ArrayExpress, ENA

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Publications


Interleukin 2 (IL-2), a cytokine linked to human autoimmune disease, limits IL-17 production. Here we found that deletion of the gene encoding the transcription factor STAT3 in T cells abrogated IL-17 production and attenuated autoimmunity associated with IL-2 deficiency. Whereas STAT3 induced IL-17 and the transcription factor RORγt and inhibited the transcription factor Foxp3, IL-2 inhibited IL-17 independently of Foxp3 and RORγt. STAT3 and STAT5 bound to multiple common sites across the locus  ...[more]

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