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STAT5 is a pioneer factor for BATF-mediated plasticity at the Il9 locus [ChIP-Seq]

ABSTRACT: BATF requires the STAT5 signal to mediate plasticity at the Il9 locus.

ORGANISM(S): Mus musculus

PROVIDER: GSE145540 | GEO | 2020/08/10

REPOSITORIES: GEO

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STAT5 is a pioneer factor for BATF-mediated plasticity at the Il9 locus [ATAC-Seq]

Project description:BATF requires the STAT5 signal to mediate plasticity at the Il9 locus.

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STAT5 is a pioneer factor for BATF-mediated plasticity at the Il9 locus [ChIP-Seq]

Project description:STAT5 is a pioneer factor for BATF-mediated plasticity at the Il9 locus [ChIP-Seq]

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STAT5 is a pioneer factor for BATF-mediated plasticity at the Il9 locus [ATAC-Seq]

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STAT5 promotes accessibility and is required for BATF-mediated plasticity at the Il9 locus

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STAT5 promotes accessibility and is required for BATF-mediated plasticity at the Il9 locus.

Project description:T helper cell differentiation requires lineage-defining transcription factors and factors that have shared expression among multiple subsets. BATF is required for development of multiple Th subsets but functions in a lineage-specific manner. BATF is required for IL-9 production in Th9 cells but in contrast to its function as a pioneer factor in Th17 cells, BATF is neither sufficient nor required for accessibility at the Il9 locus. Here we show that STAT5 is the earliest factor binding and remodeling the Il9 locus to allow BATF binding in both mouse and human Th9 cultures. The ability of STAT5 to mediate accessibility for BATF is observed in other Th lineages and allows acquisition of the IL-9-secreting phenotype. STAT5 and BATF convert Th17 cells into cells that mediate IL-9-dependent effects in allergic airway inflammation and anti-tumor immunity. Thus, BATF requires the STAT5 signal to mediate plasticity at the Il9 locus.

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Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (RNA-Seq)

Project description:Th17 cells secrete IL-17A, IL-17F, IL-21, and IL-22 cytokines that are critical in mediating inflammation and protecting the host from microorganisms infection. The basic leucine zipper transcription factor ATF-like (Batf) contributes to the transcriptional programming of multiple effector T cells, and is required for Th17 cell development. Here, we have interrogated mechanisms by which Batf promotes and stabilizes Th17 cell phenotype. We have shown that in vitro differentiated Th17 cells have increased expression of Th1 and Treg signature genes in the absence of Batf. In addition, Citrobacter rodentium infected Batf-deficient (Batf KO) mice fail to clear the infection, and that is correlated with diminished IL-17A and IL-22 cytokine production and increased Foxp3 and Ifng expression compared to WT mice. We find that Batf sustains Th17 phenotype in long-term culture conditions by suppressing Th1- and Treg-specific gene expression. Mechanistically, we reveal that Batf negatively regulates IL-2-STAT5 signaling and modulates STAT5 binding at the Ifng and Foxp3 gene loci thus suppressing Th1-Treg phenotype in Th17 cell development. Inhibition of STAT5 DNA binding activity in Batf KO Th17 cells was able to repress Ifng and Foxp3 expression compared to control-treated cells. Moreover, STAT5 cooperates with transcription factors Ets1 and Runx1 to mediate epigenetic modification and regulate gene expression. Thus, our study has revealed an essential function of Batf in modulating the IL-2-STAT5 signaling to promote and stabilize Th17 cell development.

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Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (ChIP-Seq)

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STAT5 promotes accessibility and is required for BATF-mediated plasticity at the Il9 locus

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-10 | GSE145541 | GEO

Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway

Project description:Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway

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Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (RNA-Seq)

Project description:Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (RNA-Seq)

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