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Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE250579 | GEO | 2025/05/20

REPOSITORIES: GEO

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Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression [scMultiom ATAC/RNA-seq]

Project description:TH17 cells play an important role in host defense especially in barrier organs. Altered functionality of TH17 cells is associated with dysregulated tissue homeostasis resulting in an increased susceptibility for the development of autoimmune diseases. Thus, it is critical to identify mechanisms governing physiological as well as pathophysiological TH17 cell differentiation and identify strategies targeting TH17 cell differentiation in disease settings. Here, we identified the genome organizer Special AT-rich sequence-binding protein 1 (Satb1) as a pioneering factor for TH17 cell development. Satb1 is highly expressed in TH17 cells and loss of Satb1 prevents the differentiation of TH17 cells. As a consequence, expression of Satb1 in CD4+ T cells is required for the formation of TH17 cell-driven autoimmune diseases. Mechanistically, Satb1 mediates TH17 cell development through regulating accessibility of the Il2 gene locus and thereby preventing IL-2 signaling early during TH17 cell differentiation. Thus, Satb1 is critical by suppressing IL-2 expression during the formation of TH17 cells and may be a novel therapeutic target for the treatment of TH17 cell-driven autoimmune diseases

2025-05-20 | GSE290258 | GEO

Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression

Project description:Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression

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Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression [scMultiom ATAC/RNA-seq]

Project description:Satb1 directs the differentiation of TH17 cells through suppression of IL-2 expression [scMultiom ATAC/RNA-seq]

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Suppression of SWI/SNF component Arid1a promotes mammalian regeneration through chromatin remodeling

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-03-30 | E-GEOD-76935 | biostudies-arrayexpress

TRAF6 inhibits Th17 differentiation and TGF-beta-mediated suppression of IL-2.

Project description:Transforming growth factor-beta (TGF-beta) has an essential role in the generation of inducible regulatory T (iTreg) and T helper 17 (Th17) cells. However, little is known about the TGF-beta-triggered pathways that drive the early differentiation of these cell populations. Here, we report that CD4(+) T cells lacking the molecular adaptor tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) exhibit a specific increase in Th17 differentiation in vivo and in vitro. We show that TRAF6 deficiency renders T cells more sensitive to TGF-beta-induced Smad2/3 activation and proliferation arrest. Consistent with this, in TRAF6-deficient T cells, TGF-beta more effectively down-regulates interleukin-2 (IL-2), a known inhibitor of Th17 differentiation. Remarkably, TRAF6-deficient cells generate normal numbers of Foxp3-expressing cells in iTreg differentiation conditions where exogenous IL-2 is supplied. These findings show an unexpected role for the adaptor molecule TRAF6 in Smad-mediated TGF-beta signaling and Th17 differentiation. Importantly, the data also suggest that a main function of TGF-beta in early Th17 differentiation may be the inhibition of autocrine and paracrine IL-2-mediated suppression of Th17 cell generation.

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The Satb1 protein directs hematopoietic stem cell differentiation toward lymphoid lineages.

Project description:How hematopoietic stem cells (HSCs) produce particular lineages is insufficiently understood. We searched for key factors that direct HSC to lymphopoiesis. Comparing gene expression profiles for HSCs and early lymphoid progenitors revealed that Satb1, a global chromatin regulator, was markedly induced with lymphoid lineage specification. HSCs from Satb1-deficient mice were defective in lymphopoietic activity in culture and failed to reconstitute T lymphopoiesis in wild-type recipients. Furthermore, Satb1 transduction of HSCs and embryonic stem cells robustly promoted their differentiation toward lymphocytes. Whereas genes that encode Ikaros, E2A, and Notch1 were unaffected, many genes involved in lineage decisions were regulated by Satb1. Satb1 expression was reduced in aged HSCs with compromised lymphopoietic potential, but forced Satb1 expression partly restored that potential. Thus, Satb1 governs the initiating process central to the replenishing of lymphoid lineages. Such activity in lymphoid cell generation may be of clinical importance and useful to overcome immunosenescence.

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Suppression of progenitor differentiation requires the long noncoding RNA ANCR

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Reconstruction of the dynamic regulatory network that controls Th17 cell differentiation by systematic perturbation in primary cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series