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ABSTRACT: Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells

PROVIDER: PRJNA258082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1544590.fastq.gz	Fastqsanger.gz
	SRR1544591.fastq.gz	Fastqsanger.gz
	SRR1544592.fastq.gz	Fastqsanger.gz
	SRR1544593.fastq.gz	Fastqsanger.gz
	SRR1544594.fastq.gz	Fastqsanger.gz

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Project description:Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [Affymetrix experiments]

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Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [Affymetrix experiments]

Project description:CD4+ T cells differentiate into phenotypically distinct T-helper cells upon antigenic stimulation. Regulation of plasticity between these CD4+ T-cell lineages is critical for immune homeostasis and prevention of autoimmune diseases. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARa, sustains stable expression of Th1 lineage specifying genes as well as repressing genes that instruct Th17 cell fate. RA signaling is essential for limiting Th1 cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our studies identify RA-RARa as a key component of the regulatory network governing Th1 cell fate and define a new paradigm for the development of pathogenic Th17 cells. These findings have important implications for autoimmune diseases in which dysregulated Th1-Th17 responses are observed. IFN-gamma+ Th1 cells from IFNgeYFP reporter mouse; comparing dnRARa to WT

2015-03-10 | E-GEOD-60354 | biostudies-arrayexpress

Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [ChIP-Seq experiments]

Project description:CD4+ T cells differentiate into phenotypically distinct T-helper cells upon antigenic stimulation. Regulation of plasticity between these CD4+ T-cell lineages is critical for immune homeostasis and prevention of autoimmune diseases. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARa, sustains stable expression of Th1 lineage specifying genes as well as repressing genes that instruct Th17 cell fate. RA signaling is essential for limiting Th1 cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our studies identify RA-RARa as a key component of the regulatory network governing Th1 cell fate and define a new paradigm for the development of pathogenic Th17 cells. These findings have important implications for autoimmune diseases in which dysregulated Th1-Th17 responses are observed. Identification of RARa binding in wild-type Th1 cells and mapping of enhancers using chromatin IP against p300, H3k4me1, H3k4me3, and H3k27ac in wild-type and dnRara Th1 cells.

2015-03-10 | E-GEOD-60353 | biostudies-arrayexpress

Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [Agilent experiments]

2015-03-10 | GSE60355 | GEO

Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [Affymetrix experiments]

2015-03-10 | GSE60354 | GEO

Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [ChIP-Seq experiments]

2015-03-10 | GSE60353 | GEO

Population RNA-seq of in vitro polarized CD4 T cells

Project description:To understand the molecular programs driving Th17 heterogeneity and CD4 T cell fate, we profiled in vitro polarized non-pathogenic Th17, pathogenic Th17, Th1, and Treg cells using RNA-seq.

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Single-cell RNA-seq and single-cell ATAC-seq of in vitro polarized mouse Th17 and Th1 cells

Project description:We generated droplet-based single-cell RNA-seq profiles of non-pathogenic Th17, pathogenic Th17, and Th1 cells after 48 hours in polarization conditions

2023-06-01 | GSE206175 | GEO

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