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Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

ABSTRACT: To investigate the role of IkE5 in Treg cell biology, we established IkE5-deficient Treg cells from Foxp3-Cre IkE5 floxed mice. We then performed assay for transposase-accessible chromatin (ATAC)-seq to evaluate the chromatin accessibility in wild-type and IkE5-deficient Treg cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE229588 | GEO | 2024/08/07

REPOSITORIES: GEO

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Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:To investigate the role of IkE5 in Treg cell biology, we established IkE5-deficient Treg cells from Foxp3-Cre IkE5 floxed mice. We then performed gene expression profiling analysis using data obtained from bulk RNA-seq of wild-type and IkE5-deficient Treg cells.

2024-08-07 | GSE229591 | GEO

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

Project description:To investigate the role of IkE5 in Treg cell biology, we established IkE5-deficient Treg cells from Foxp3-Cre IkE5 floxed mice. We then performed Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for several transcription factors and epigenetic regulators as well as the histone modification H3K27ac in wild-type and IkE5-deficient Treg cells.

2024-08-07 | GSE229590 | GEO

Transcription factor Ikzf1 associates with Foxp3 to repress gene expression in Treg cells and limit autoimmunity and anti-tumor immunity

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

2024-08-07 | GSE229592 | GEO

FOXP3 exon 2 controls Treg stability and autoimmunity [RNA-seq]

Project description:Differing from the mouse Foxp3 gene that encodes only one protein product, human FOXP3 encodes two major isoforms through alternative splicing – a longer isoform (FOXP3 FL) containing all the coding exons and the other shorter isoform lacking the amino acids encoded by exon 2 (FOXP3 ΔE2). The two isoforms are naturally expressed in humans yet their differences in controlling regulatory T cell phenotype and functionality remains unclear. Here we show that patients expressing only the shorter isoform failed to maintain self-tolerance and developed IPEX syndrome. Mice with Foxp3 exon 2 deletion developed excessive TFH and GC B cell responses and systemic autoimmune disease with anti-dsDNA and anti-nuclear autoantibody production and immune-complex glomerulonephritis. Regulatory T cells expressing FOXP3 ΔE2 were unstable and sufficient to induce autoimmunity when transferred into Tcrb-deficient mice. Mechanistically, FOXP3 ΔE2 isoform allows increased expression of selected cytokines but decreased expression of a set of Foxp3 positive regulators without altered binding to these gene loci. We demonstrate that exon 2 of FOXP3 is required to maintain Treg stability and immune homeostasis.

2022-06-27 | GSE199477 | GEO

FOXP3 exon 2 controls Treg stability and autoimmunity [ChIP-seq]

2022-06-27 | GSE199277 | GEO

FOXP3 exon 2 controls Treg stability and autoimmunity

Project description:FOXP3 exon 2 controls Treg stability and autoimmunity

| PRJNA820377 | ENA

FoxP3 associates with enhancer-promoter loops to regulate Treg-specific gene expression [HiChIP]

Project description:We applied proximity-ligation with chromatin immunoprecipitation (HiChIP) in Treg and closely related conventional CD4+ T cells (Tconv) to map the H3K27Ac, FoxP3 and Yy1 chromatin structures.

2021-11-26 | GSE189442 | GEO

Transcriptional profiling of FOXP3+ Treg cells and corresponding FOXP3-losing cells

Project description:Natural CD4+FOXP3+ regulatory T (Treg) cells constitute a unique T-cell lineage that plays a pivotal role in maintaining immune homeostasis and immune tolerance. Recent studies provide evidence for the heterogeneity and plasticity of the Treg cell lineage. However, the fate of human Treg cells after loss of FOXP3 expression and the underlying epigenetic mechanisms remain to be fully elucidated. Here, we compared gene expression profiles and histone methylation status on two histone H3 lysine residues (H3K4me3 and H3K27me3) of expanded FOXP3+ and corresponding FOXP3-losing Treg cells. DGE assay showed that human Treg cells down-regulated Treg signature genes, whereas up-regulated a set of Th lineages-associated genes, especially for Th2, such as GATA3, GFI1 and IL13, after in vitro expansion. Furthermore, we found that reprogramming of Treg cells was associated with histone modifications, as shown by decreased abundance of permissive H3K4me3 within down-regulated Treg signature genes, such as FOXP3, CTLA4 and LRRC32 loci, although with no significant changes in H3K27me3 modification. Thus, our results indicate that human Treg cells could convert into a Th-like cells upon in vitro expansion, displaying a gene expression signature dominated by Th2 lineage associated genes, and the histone methylation might contribute to such conversion. mRNA profiles of in-vitro-expanded FOXP3+ Treg and FOXP3-losing Treg cells generated by deep sequencing.

2013-06-06 | E-GEOD-47636 | biostudies-arrayexpress

Blimp1 is required to repress Foxp3+ regulatory T cell pathogenic activity in mice

Project description:Foxp3+Tregcells are essential modulators of immune responses but under specific conditions can acquire inflammatory properties and potentially contribute to disease pathogenesis. Here we show that the transcription factor Blimp1 is a critical regulator of Foxp3+Treg functional plasticity. The intrinsic expression of Blimp1 was required to prevent Treg from producing Th17-associated cytokines and acquiring an inflammatory phenotype while preserving Foxp3 expression. Mechanistically, Blimp1 acts as a direct repressor of the Il17a/Il17f genes in Foxp3+Treg and binding of Blimp1 at this locus is associated with altered chromatin status, reduced binding the co-activator p300, unaltered binding of the Th17-asssociated transcription factor RORt and more abundant binding of IRF4, which was required for the production of IL17A in Blimp1-deficient Foxp3+Tregcells, as shown by IRF4 siRNA-mediated knockdown. Consistent with their capacity to produce inflammatory cytokines, Blimp1-deficient Foxp3+Treg exacerbate Th17-mediated inflammation in vivo indicating that Blimp1 is required to prevent Treg cells from acquiring pathogenic properties

2019-01-08 | GSE84827 | GEO

Gene expression profiles of Foxp3RFP (WT), Foxp3∆EGFPiCre (Foxp3-deficient) and Foxp3∆EGFPiCreRictor∆/∆ (Foxp3-deficient and Rictor deficient) Treg cells.

Project description:Comparaison of the transcriptomes of WT and Foxp3-deficient regulatory T cells from the spleen of females that carried one mutant Foxp3∆EGFPiCre allele and a second competent Foxp3 allele (Foxp3RFP) that also directed the expression of the red fluorescent protein (RFP) . We then extended these studies to elucidate transcriptional pathways altered upon Rictor deletion in ∆Treg cells that may contribute to their improved regulatory function by analyzing the transcriptome of ∆Treg cells isolated from Foxp3∆EGFPiCre/+Rictor∆/∆ females.

2019-04-08 | GSE129472 | GEO

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