Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (bulk RNA)

ABSTRACT: Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (bulk RNA)

PROVIDER: PRJNA636406 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11903500_1.fastq.gz	Fastqsanger.gz
	SRR11903500_2.fastq.gz	Fastqsanger.gz
	SRR11903501_1.fastq.gz	Fastqsanger.gz
	SRR11903501_2.fastq.gz	Fastqsanger.gz
	SRR11903502_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 144

Similar Datasets

Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions

Project description:Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions

| PRJNA639610 | ENA

Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (single-cell RNA)

Project description:Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (single-cell RNA)

| PRJNA638640 | ENA

Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions

Project description:Comparing the transcriptomic program induced by oleic acid to that of the pro-inflammatory arachidonic acid, we find that Tregs sorted from peripheral blood and adipose of healthy donors transcriptomically resemble the oleic acid in vitro treated Tregs, whereas Tregs obtained from the adipose tissue of relapsing-remitting MS patients more closely resemble an arachidonic acid profile

2020-11-17 | GSE152543 | GEO

Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (bulk RNA)

2020-11-17 | GSE151586 | GEO

Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (single-cell RNA)

2020-11-17 | GSE152197 | GEO

Transcriptional correlates of FOXP3 expression in suppressive and non-suppressive primary human Treg cell clones.

Project description:Analysis of the transcriptional correlates of FOXP3 expression in suppressive and non-suppressive primary human Treg cell clones. Individual CD4+CD25High or Cd4+CD25- T cells were isolated from human PBMCs and expanded in vitro. After 3 weeks of expansion, individual clones were analysed for FOXP3 expression and in vitro suppressive activity against freshly sorted allogeneic effector T cells. This study analyses the total RNA isolated from FOXP3+ clones with suppressive potency to their non-suppressive counterparts. The resutls of this study should provide insights into the molecular pathways linking FOXP3 expression to distinct aspects of Treg phenotype and function. Total RNA obtained from individual clones of primary human regulatory and effector CD4+T cells.

2015-05-06 | E-GEOD-65650 | biostudies-arrayexpress

Transcriptional correlates of FOXP3 expression in suppressive and non-suppressive primary human Treg cell clones.

2015-05-06 | GSE65650 | GEO

Oleic acid restores suppressive defects in tissue-resident FOXP3 Tregs from patients with multiple sclerosis.

Project description:FOXP3+ Tregs rely on fatty acid β-oxidation-driven (FAO-driven) oxidative phosphorylation (OXPHOS) for differentiation and function. Recent data demonstrate a role for Tregs in the maintenance of tissue homeostasis, with tissue-resident Tregs possessing tissue-specific transcriptomes. However, specific signals that establish tissue-resident Treg programs remain largely unknown. Tregs metabolically rely on FAO, and considering the lipid-rich environments of tissues, we hypothesized that environmental lipids drive Treg homeostasis. First, using human adipose tissue to model tissue residency, we identified oleic acid as the most prevalent free fatty acid. Mechanistically, oleic acid amplified Treg FAO-driven OXPHOS metabolism, creating a positive feedback mechanism that increased the expression of FOXP3 and phosphorylation of STAT5, which enhanced Treg-suppressive function. Comparing the transcriptomic program induced by oleic acid with proinflammatory arachidonic acid, we found that Tregs sorted from peripheral blood and adipose tissue of healthy donors transcriptomically resembled the Tregs treated in vitro with oleic acid, whereas Tregs from patients with multiple sclerosis (MS) more closely resembled an arachidonic acid transcriptomic profile. Finally, we found that oleic acid concentrations were reduced in patients with MS and that exposure of MS Tregs to oleic acid restored defects in their suppressive function. These data demonstrate the importance of fatty acids in regulating tissue inflammatory signals.

| S-EPMC7810477 | biostudies-literature

Foxp3 enhancers synergize to maximize regulatory T cell suppressive capacity [Bisulfite-Seq]

Project description:Treg cells bearing a diverse antigen receptor repertoire suppress pathogenic T cells and maintain immune homeostasis during their long lifespan. How their robust function is determined genetically remains elusive. Here, we investigate the regulatory space of the cis-regulatory elements of Treg lineage–specifying factor Foxp3. Foxp3 enhancers are known as distinct readers for environmental cues in promoting Treg cell induction or lineage stability. However, their single deficiencies cause mild, if any, immune dysregulation, leaving the key transcriptional mechanisms determining Foxp3 expression and thereby Treg suppressive capacity uncertain. We examined the collective activities of Foxp3 enhancers and found that they coordinate to maximize Treg cell induction, Foxp3 expression level, or lineage stability through distinct modes and that ablation of synergistic enhancers led to lethal autoimmunity in young mice. Thus, the induction and maintenance of a diverse, stable Treg cell repertoire rely on combinatorial Foxp3 enhancers, suggesting broad, stage-specific, synergistic activities of cell-intrinsic factors and -extrinsic cues in determining Treg suppressive capacity.

2021-05-10 | GSE158222 | GEO