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Dynamic Foxp3-chromatin interaction controls tunable Treg cell function [RNA-seq Foxp3 KO]

ABSTRACT: Dynamic Foxp3-chromatin interaction controls tunable Treg cell function [RNA-seq Foxp3 KO]

PROVIDER: PRJNA1026941 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26360152_1.fastq.gz	Fastqsanger.gz
	SRR26360152_2.fastq.gz	Fastqsanger.gz
	SRR26360153_1.fastq.gz	Fastqsanger.gz
	SRR26360153_2.fastq.gz	Fastqsanger.gz
	SRR26360154_1.fastq.gz	Fastqsanger.gz

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Dynamic Foxp3-chromatin interaction controls tunable Treg cell function

Project description:Dynamic Foxp3-chromatin interaction controls tunable Treg cell function

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Dynamic Foxp3-chromatin interaction controls tunable Treg cell function [RNA-seq Foxp3 KO]

Project description:Nuclear factor Foxp3 determines regulatory T (Treg) cell fate and function via mechanisms that remain unclear. Here we investigate the nature of Foxp3-mediated gene regulation in suppressing autoimmunity and antitumor immune response. Contrasting with previous models, we find that Foxp3-chromatin binding is regulated by Treg activation states, tumor microenvironment, and antigen and cytokine stimulations. Proteomics studies uncovered dynamic proteins within the Foxp3 proximity upon TCR or IL-2 receptor signaling in vitro, reflecting intricate interactions among Foxp3, signal transducers, and chromatin. Pharmacological inhibition and genetic knockdown experiments indicate that NFAT and AP-1 protein Batf are required for enhanced Foxp3-chromatin binding in activated Treg cells and tumor-infiltrating Treg cells to modulate target gene expression. Furthermore, mutations at Foxp3 DNA-binding domain destabilize Foxp3-chromatin association. These representative settings delineate context-dependent Foxp3-chromatin interaction, suggesting that Foxp3 associates with chromatin by hijacking DNA-binding proteins resulting from Treg activation or differentiation, which is stabilized by direct Foxp3-DNA binding, to dynamically regulate Treg cell function according to immunological contexts.

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Dynamic Foxp3-chromatin interaction controls tunable Treg cell function [Cut&Tag Foxp3]

Project description:Dynamic Foxp3-chromatin interaction controls tunable Treg cell function [Cut&Tag Foxp3]

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Dynamic Foxp3-chromatin interaction controls tunable Treg cell function

Project description:This SuperSeries is composed of the SubSeries listed below. Nuclear factor Foxp3 determines regulatory T (Treg) cell fate and function via mechanisms that remain unclear. Here we investigate the nature of Foxp3-mediated gene regulation in suppressing autoimmunity and antitumor immune response. Contrasting with previous models, we find that Foxp3-chromatin binding is regulated by Treg activation states, tumor microenvironment, and antigen and cytokine stimulations. Proteomics studies uncovered dynamic proteins within the Foxp3 proximity upon TCR or IL-2 receptor signaling in vitro, reflecting intricate interactions among Foxp3, signal transducers, and chromatin. Pharmacological inhibition and genetic knockdown experiments indicate that NFAT and AP-1 protein Batf are required for enhanced Foxp3-chromatin binding in activated Treg cells and tumor-infiltrating Treg cells to modulate target gene expression. Furthermore, mutations at Foxp3 DNA-binding domain destabilize Foxp3-chromatin association. These representative settings delineate context-dependent Foxp3-chromatin interaction, suggesting that Foxp3 associates with chromatin by hijacking DNA-binding proteins resulting from Treg activation or differentiation, which is stabilized by direct Foxp3-DNA binding, to dynamically regulate Treg cell function according to immunological contexts.

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Dynamic Foxp3-chromatin interaction controls tunable Treg cell function [Cut&Run Foxp3 Batf]

Project description:Dynamic Foxp3-chromatin interaction controls tunable Treg cell function [Cut&Run Foxp3 Batf]

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