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- W4313374508 abstract "Abstract The Ikaros zinc finger (IkZF) transcription factor Eos is a known regulator of CD4+ regulatory T cell (TREG) populations. However, its role in the differentiation of other CD4+ T cell subsets is unknown. Here, we find that Eos deficiency results in both compromised TH1 cell differentiation and reduced production of the TH1 effector cytokine IFN-γ. Historically, IkZF factors have been associated with changes in gene expression via the alteration of chromatin structure. However, ATAC-seq analysis indicated that there were minimal changes in chromatin accessibility between wild type and Eos-deficient cells cultured under TH1-polarizing conditions. Rather, we find that IL-2 signaling promotes the STAT5-dependent induction of Eos expression, and that Eos both interacts with STAT5 and supports tyrosine phosphorylation-mediated STAT5 activation. Consequently, STAT5 enrichment is reduced at TH1 target genes in the absence of Eos. Thus, modulation of STAT5 signaling represents a novel mechanism by which Eos positively regulates the TH1 gene program. Given the important role for IL-2/STAT5 signaling in the differentiation of TH2, TH9, and TREG cell subsets, it will be of interest to determine whether this mechanism is conserved across additional CD4+ T cell populations." @default.
- W4313374508 created "2023-01-06" @default.
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- W4313374508 date "2020-05-01" @default.
- W4313374508 modified "2023-10-12" @default.
- W4313374508 title "Eos supports TH1 differentiation through feed-forward propagation of the IL-2/STAT5 signaling pathway" @default.
- W4313374508 doi "https://doi.org/10.4049/jimmunol.204.supp.76.18" @default.
- W4313374508 hasPublicationYear "2020" @default.
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