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Genome wide chromatin accessibility (ATAC-SEQ) in the presence or absence of Ikaros in CD4+ T cells.

ABSTRACT: Genome wide chromatin accessibility (ATAC-SEQ) in the presence or absence of Ikaros in CD4+ T cells.

PROVIDER: PRJNA662893 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12623426_1.fastq.gz	Fastqsanger.gz
	SRR12623426_2.fastq.gz	Fastqsanger.gz
	SRR12623427_1.fastq.gz	Fastqsanger.gz
	SRR12623427_2.fastq.gz	Fastqsanger.gz
	SRR12623428_1.fastq.gz	Fastqsanger.gz

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CD4+ T cells in presence or absence of Ikaros

Project description:CD4+ T cells in presence or absence of Ikaros

| PRJNA662885 | ENA

Genome wide chromatin accessibility (ATAC-SEQ) in the presence or absence of Ikaros in CD4+ T cells.

Project description:We found that Ikaros is critical to limit the expression of pro-inflammatory cytokines in TCR/CD28-activated CD4+ T cells. To understand if Ikaros could modify the chromatin accessibility in regions controling the expression of these pro-inflammatory genes, we examined the chromatin state in naive CD4+ T cells and CD4+ T cells activated with anti-CD3+anti-CD28 antibodies for 1 and 2 days, from WT (Ikaros f/f CD4-Cre-) and Ikaros TKO mice (Ikaros f/f CD4-Cre+), using the ATAC-seq approach.

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RNA-SEQ analysis of CD4+ T cells in presence or absence of Ikaros.

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RNA-SEQ analysis of CD4+ T cells in presence or absence of Ikaros.

Project description:We found by microarray analysis that Ikaros is critical to limit the expression of several pro-inflammatory genes during Th17 cell polarization. To unravel the role of Ikaros in the expression of pro-inflammatory genes without Th17 polarizing cytokines, we performed an RNA-seq analysis in naive CD4+ T cells and CD4+ T cells activated with anti-CD3+anti-CD28 antibodies (Th0 condition), from WT (Ikaros f/f CD4-Cre-) and Ikaros TKO mice (Ikaros f/f CD4-Cre+).

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Transcriptome profiling of mouse CD4+ T cells in the presence or absence of acetate

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Genome-wide binding of Ikaros in naive CD4+ T cells and Th0 at day1

Project description:The aim of the project is to determine the binding sites of Ikaros in CD4+ T cells. To perform this, CD4 naive T cells (CD4 TN; d0) either rested or activated with anti-CD3+anti-CD28 Abs for 1 day (Th0 d1) were subjected to a ChIP using anti-Ikaros Ab followed by high throughput sequencing.

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Ikaros/STAT5 DNA binding competition in pre-B cell line [ChIP-seq]

Project description:Ikaros was found to antagonize the transcriptional program of IL-7 activated pathways during pre-B cell differentiation. We analyzed the genomic distribution of Ikaros and STAT5 (downstream effector of IL-7; in the presence or absence of Ikaros) in pre-B cells by ChIP-Seq.

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Effect of Ikaros deletion on gene expression in CD4 T cells

Project description:The goal of this experiment is to define how lack of Ikaros impacts gene expression in mature CD4 T cells, both in the resting and activated state. To do this, a conditional knockout mouse model was generated using Cre/lox technology. The floxed allele was designed such that the last translated exon and 3' UTR of the Ikaros gene (Ikzf1) are deleted in mature T cells (mediated by distal Lck-driven Cre). CD4 T cells from mice with floxed alleles that did not express Cre (Cre-) and those that did express Cre (Cre+) were analyzed.

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Expression data from CD4+ Naïve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shapes gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms has not yet been unknown. To reveal the mechanism, we isolated Naïve CD4+ T cells from spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria.

2013-11-20 | GSE49619 | GEO

Expression data from CD4+ naïve T cells under Treg-inducing condition in the presence or absence of butyrate

Project description:Commensal bacteria shape the gut immune system. Colonization bacteria increase the frequency of regulatory T cells, however, the molecular mechanisms are not yet known. To reveal the mechanism, we isolated naïve CD4+ T cells from the spleen of C57BL/6 mice and cultured the cells under Treg-inducing condition culture in the presence or absence of butyrate, a metabolite produced by commensal bacteria.

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