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Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [ATAC-Seq]

ABSTRACT: Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [ATAC-Seq]

PROVIDER: PRJNA823556 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18636088_1.fastq.gz	Fastqsanger.gz
	SRR18636088_2.fastq.gz	Fastqsanger.gz
	SRR18636089_1.fastq.gz	Fastqsanger.gz
	SRR18636089_2.fastq.gz	Fastqsanger.gz
	SRR18636090_1.fastq.gz	Fastqsanger.gz

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Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [ATAC-Seq]

Project description:We investigated the role of Ikaros in regulatory Tcell identity and function during stimulation using RNA-seq, ATAC-seq, and H3K27ac/Foxp3/Ikzf1 ChIP-seq

2024-03-28 | GSE200176 | GEO

Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [RNA-Seq]

Project description:We investigated the role of Ikaros in regulatory Tcell identity and function during stimulation using RNA-seq, ATAC-seq, and H3K27ac/Foxp3/Ikzf1 ChIP-seq

2024-03-28 | GSE200178 | GEO

Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [ChIP-Seq]

Project description:We investigated the role of Ikaros in regulatory Tcell identity and function during stimulation using RNA-seq, ATAC-seq, and H3K27ac/Foxp3/Ikzf1 ChIP-seq

2024-03-28 | GSE200177 | GEO

Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function

Project description:Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function

| PRJNA823549 | ENA

Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [ChIP-Seq]

Project description:Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [ChIP-Seq]

| PRJNA823555 | ENA

Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [RNA-Seq]

Project description:Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function [RNA-Seq]

| PRJNA823557 | ENA

Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function.

Project description:Ikaros is a transcriptional factor required for conventional T cell development, differentiation, and anergy. While the related factors Helios and Eos have defined roles in regulatory T cells (Treg), a role for Ikaros has not been established. To determine the function of Ikaros in the Treg lineage, we generated mice with Treg-specific deletion of the Ikaros gene (Ikzf1). We find that Ikaros cooperates with Foxp3 to establish a major portion of the Treg epigenome and transcriptome. Ikaros-deficient Treg exhibit Th1-like gene expression with abnormal production of IL-2, IFNg, TNFa, and factors involved in Wnt and Notch signaling. While Ikzf1-Treg-cko mice do not develop spontaneous autoimmunity, Ikaros-deficient Treg are unable to control conventional T cell-mediated immune pathology in response to TCR and inflammatory stimuli in models of IBD and organ transplantation. These studies establish Ikaros as a core factor required in Treg for tolerance and the control of inflammatory immune responses.

| S-EPMC11042806 | biostudies-literature

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ATAC-Seq]

Project description:Using patient-derived Ph+ pre-B ALL cells that harbor deletions of the IKZF1 DNA binding domain (Ik6), we performed ATAC-sequencing in cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

2017-02-06 | GSE90666 | GEO

Foxp3 depends on Ikaros for control of regulatory T cell gene expression and function

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

2024-03-28 | GSE200179 | GEO

Mbd2 promotes Foxp3 demethylation and T-regulatory cell function

Project description:The proposed use of Foxp3+ T-regulatory (Treg) cells as potential cellular therapy in patients with autoimmune diseases, or post-hemopoietic stem cell or organ transplantation, requires a sound understanding of the transcriptional regulation of Foxp3 expression. Conserved CpG dinucleotides in the Treg-specific demethylated region (TSDR) upstream of Foxp3 are demethylated only in stable, thymic-derived Foxp3+ Tregs. Since methyl-binding domain (Mbd) proteins recruit histone-modifying and chromatin-remodeling complexes to methylated sites, we tested whether targeting of Mbd2 might promote demethylation of Foxp3 and thereby promote Treg numbers or function. Surprisingly, while ChIP analysis showed Mbd2 binding to the Foxp3-associated TSDR site in Tregs, Mbd2 targeting by homologous recombination or siRNA decreased Treg numbers and impaired Treg suppressive function in vitro and in vivo. Moreover, we found complete TSDR demethylation in WT Tregs but >75% methylation in Mbd2-/- Tregs, whereas re-introduction of Mbd2 into Mbd2-null Tregs restored TSDR demethylation, Foxp3 gene expression and Treg suppressive function. Lastly, Mbd2-/- Tregs had markedly binding of the DNA demethylase enzyme, Tet2, in the TSDR region. These data show that Mbd2 has a key role in promoting TSDR demethylation, Foxp3 expression and Treg suppressive function. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of MBD2–/– mice, compared to wild type control (all Balb/c background).

2013-09-01 | E-GEOD-48653 | biostudies-arrayexpress

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