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

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

PROVIDER: PRJNA823555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18636500_1.fastq.gz	Fastqsanger.gz
	SRR18636500_2.fastq.gz	Fastqsanger.gz
	SRR18636501_1.fastq.gz	Fastqsanger.gz
	SRR18636501_2.fastq.gz	Fastqsanger.gz
	SRR18636502_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

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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

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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

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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

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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]

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

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

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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

Foxp3+ regulatory T cells control hypothalamic inflammation

Project description:The central nervous system (CNS) hypothalamus controls systemic metabolism. Inflammatory CNS processes evolving upon exposure to calorie-rich diet are thought to promote impaired metabolic CNS control, thereby triggering obesity and Type-2 diabetes (T2D). However, immune cells relevant for maintaining hypothalamic integrity remain incompletely understood. Here, we identify hypothalamic CD4+Foxp3+regulatory T(Treg) cells which control local tissue-inflammation. Specifically, upon exposure to a calorie-rich diet, a significant decline in hypothalamus-residing Foxp3+Tregs occurred and was accompanied by increased immune activation of CD4+T cells, infiltrating macrophages and microglia. Microglial proteomes of mice exposed to the hypercaloric challenge confirmed characteristics of immune activation; specifically, mRNA expression profiling of hypothalamic CD4+T cells indicated a Th1-mediated inflammatory state evidenced by high levels of Tbx21, Cxcr3, Cd226 and reduced expression of Ccr7 and S1P1 receptors relevant for recruitment to and retention at inflammatory sites. Using Treg depletion and transfer experiments in vivo, we found that Foxp3+Tregs critically limit hypothalamic immune activation induced by hyper-caloric challenge. Our findings open new avenues in the design of tailored concepts to improve immunometabolic health in obesity and T2D.

2025-01-20 | PXD004498 | Pride

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

Loss of Foxp3-driven epigenetic modification leads to regulatory T cell insufficiency

Project description:Regulatory T cells (Tregs) are responsible for limiting autoimmunity and chronic inflammation. Foxp3 is a transcription factor that acts as a master regulator of Treg development and function. A serendipitous observation led to the realization that a well-characterized Foxp3gfp reporter mouse, which expresses an N-terminal GFP-Foxp3 fusion protein, is a hypomorph that causes profoundly accelerated autoimmune diabetes on a NOD background. Although natural Treg development and in vitro function is not significantly altered in Foxp3gfp NOD and C57BL/6 mice, Treg fitness function in inflammatory environments is perturbed and TGF?-induced Treg development reduced. Foxp3gfpis unable to interact with the histone acetyltransferase Tip60, the histone deacetylase HDAC7, and the Ikaros family zinc finger 4, Eos, which leads to reduced Foxp3 acetylation and enhanced K48-linked polyubiquitylation. Collectively this leads to an altered transcriptional landscape and reduced Foxp3-mediated gene repression, notably at the hallmark IL-2 promoter. Loss of controlled Foxp3-driven epigenetic modification leads to Treg insufficiency that causes autoimmunity in prone environments. 16 samples overall split between 2 genotypes (wild type and Foxp3 knock in) and two cell types (Tregs and Tconv)

2012-12-07 | E-GEOD-35164 | biostudies-arrayexpress

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