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Runx3 drives a tissue residency program that is absent in CD4+ T cells [ATAC-seq]

ABSTRACT: Runx3 drives a tissue residency program that is absent in CD4+ T cells [ATAC-seq]

PROVIDER: PRJNA816148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18326739_1.fastq.gz	Fastqsanger.gz
	SRR18326739_2.fastq.gz	Fastqsanger.gz
	SRR18326740_1.fastq.gz	Fastqsanger.gz
	SRR18326740_2.fastq.gz	Fastqsanger.gz
	SRR18326741_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Runx3 drives a tissue residency program that is absent in CD4+ T cells [ATAC-seq]

Project description:Tissue-resident memory T (TRM) cells provide rapid and superior control of localized infections. The transcription factor Runx3 was recently identified as a master regulator of CD8+ T cell tissue residency. However, Runx3 also drives CD8+ T cell lineage commitment and is repressed in CD4+ T cells, raising the possibility that this transcription factor defines a form of tissue residency unique to the CD8+ T cell subset. Here, we show that as a direct consequence of Runx3-deficiency, CD4+ TRM cells in epithelia lack the TGFb-responsive transcriptional network that underpins CD8+ TRM cell residency. Ectopic Runx3 expression in CD4+ T cells rescued this transcriptional program to promote prolonged survival, decreased tissue egress and a microanatomical redistribution towards epithelial layers that combined, resulted in superior local immune protection. Our results thus reveal a mechanistic discordance between CD4+ and CD8+ TRM cell formation in barrier tissues that is controlled by Runx3. Consequently, CD4+ TRM cells are unable to adopt a type of tissue residency that is intrinsically accessible to the CD8+ TRM cell subset.

2022-05-24 | GSE198611 | GEO

Runx3 drives a tissue-residency program that is absent in CD4+ T cells

Project description:Runx3 drives a tissue-residency program that is absent in CD4+ T cells

| PRJNA816144 | ENA

Runx3 drives a tissue-residency program that is absent in CD4+ T cells [RNA-seq]

Project description:Pattens of tissue-residency differs between CD4+ and CD8+ memory T cells in evironmentally exposed organs. The lineage-controlling transcription factor Runx3, expressed in CD8+ T cells, is responsible for shaping a tissue-resident gene network in response to the cytokine TGF-b. While the lack of Runx3 by CD4+ T cells precludes these transcriptional changes, Runx3-overexpression in CD+ T cells enable phenotypical, transcriptional and functional changes to allow residency.

2022-05-24 | GSE182511 | GEO

Runx3 drives a tissue-residency program that is absent in CD4+ T cells [RNA-seq]

Project description:Runx3 drives a tissue-residency program that is absent in CD4+ T cells [RNA-seq]

| PRJNA756546 | ENA

Hepatic leukemia factor directs tissue residency of proinflammatory CD4+ T cells

Project description:CD4+ tissue-resident memory T cells (TRM) contribute to both host defense and pathogenesis of chronic inflammatory diseases. However, the molecular mechanisms that direct tissue residency and functional heterogeneity of CD4+ TRM remain unknown. We herein show that the transcription factor, hepatic leukemia factor (HLF), directs the tissue residency program and functionality of CD4+ TRM. HLF simultaneously upregulates tissue retention receptors and downregulates tissue egress receptors via changes in chromatin accessibility, and drives proinflammatory CD4+ TRM by inducing Bhlhe40. Genetic deletion of Hlf inhibits CD4+ TRM generation, consequently ameliorating airway tissue inflammation in vivo. In humans, HLF-positive CD4+ TRM from inflamed airway tissue have a tissue residency signature and express inflammatory cytokines. HLF is therefore a central regulator of proinflammatory CD4+ TRM development and function.

2025-07-04 | GSE295436 | GEO

Hepatic leukemia factor directs tissue residency of proinflammatory CD4+ T cells [bulk]

2025-07-04 | GSE295553 | GEO

Runx3 function in CD4+ splenic dendritic cells

Project description:CD4+ dendritic cells are part of the innate immunity essential for priming and activating of CD4+ T cells To identify Runx3 responsive genes CD4+ dendritic cells were sorted from freshly isolated macs enriched splenic DCs taken from 6 weeks old mice. Six samples from six mice were sorted and analyzed where in each littermates pair consisted of a control and Runx3 KO.

2014-06-22 | E-GEOD-48589 | biostudies-arrayexpress

Runx3 drives a tissue-residency program that is absent in CD4+ T cells

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

2022-05-24 | GSE198612 | GEO

Genome-wide maps of Runx3 bound regions in CD4 splenic dendritic cells.

Project description:ChIP-seq was conducted using FACS-isolated CD11chiMHCII+CD4+ splenic WT DC and anti-Runx3 antibodies (Ab). Two biological Runx3 IP repeats and two input controls from sorted CD4 DC

2014-06-22 | E-GEOD-48588 | biostudies-arrayexpress

The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

2019-11-12 | PXD007511 | Pride

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