Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Sumoylation of RORgt controls TH17 differentiation and thymocyte development

PROVIDER: PRJNA477225 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7403100.fastq.gz	Fastqsanger.gz
	SRR7403110.fastq.gz	Fastqsanger.gz
	SRR7403091.fastq.gz	Fastqsanger.gz
	SRR7403101.fastq.gz	Fastqsanger.gz
	SRR7403092.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Decoupling the role of RORγt in the differentiation and effector function of Th17 cells

Project description:RORgt is known to instruct the differentiation of Th17 cells that mediate the pathogenesis of autoimmune diseases. However, it remains unknown whether RORgt plays a distinct role in the differentiation and effector function of Th17 cells. Here we show that mutation of RORgt lysine 256, a ubiquitination site, to arginine (K256R) separates the RORgt role in these two functions. Preventing ubiquitination at K256 via arginine substitution does not affect RORgt-dependent thymocyte development and Th17 differentiation in vitro and in vivo, however, greatly impaired the pathogenesis of Th17 cell-mediated experimental autoimmune encephalomyelitis (EAE). Mechanistically, K256R mutation impairs RORgt to bind to and activate Runx1 expression critical for Th17-mediated EAE. Thus, RORgt regulates the effector function of Th17 cells in addition to Th17 differentiation. This work informs the development of RORgt-based therapies that specifically target the effector function of Th17 cells responsible for autoimmunity.

2022-10-26 | GSE211414 | GEO

Decoupling the role of RORgt in the differentiation and effector function of Th17 cells

2022-10-26 | GSE211509 | GEO

Mus musculus strain:mouse

Project description:RORgt function in Th17 differentiation but not thymocyte development

| PRJNA382873 | ENA

ChIP-Seq analysis C57BL/6 thymocytes

Project description:In this study, we show that in addition to regulating DP thymocytes survival, RORgT also controls genes that regulate thymocyte migration, proliferation, and T cell receptor (TCR) selection. Strikingly, pharmacological inhibition of RORg skews TCR gene rearrangement, limits T cell repertoire diversity, and inhibits development of autoimmune encephalomyelitis. Thus, targeting RORgT not only inhibits Th17 cell development and function but also fundamentally alters thymic-emigrant recognition of self and foreign antigens.

2016-10-20 | GSE88916 | GEO

Project description:Selective inhibition of RORgt-dependent Th17 differentiation but not thymocyte development by IMU-935

| PRJNA1297911 | ENA

Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation [ChIP-seq]

Project description:Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

2017-10-25 | GSE101593 | GEO

Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation

Project description:Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

2017-10-25 | GSE101527 | GEO

ATAC-seq of wild type and Stat3-deficient or Rorgt-deficient Th17 cells

Project description:STAT3 has a more profound effect on chromatin accessibility regulation than RORgt during Th17 cell differentiation.

2020-07-30 | GSE153442 | GEO

Genetic and pharmacological inhibition of the nuclear receptor RORa regulates Th17 driven inflammatory disorders

Project description:Full development of IL-17 producing CD4+ T helper cells (TH17 cells) requires the transcriptional activity of both orphan nuclear receptors RORa and RORgt. Despite this evidence, RORa is considered functionally redundant to RORgt; thus, the function and therapeutic value of RORa in TH17 cells remains underexplored. Using mouse models of autoimmune and chronic inflammation, we show that expression of RORa is required for TH17 cell pathogenicity. T-cell specific deletion of RORa reduced the development of experimental autoimmune encephalomyelitis (EAE) and colitis. Reduced inflammation was associated with decreased TH17 cell development, lower expression of tissue-homing chemokine receptors and integrins, and increased frequencies of Foxp3+ T regulatory (Treg) cells. Importantly, inhibition of RORa with a selective small molecule antagonist largely phenocopied our genetic data, potently suppressing the in vivo development of both chronic/progressive and relapsing/remitting EAE but had no effect on overall thymic cellularity. Furthermore, use of the RORa antagonist effectively inhibited human TH17 cell differentiation and memory cytokine secretion. Together, these data suggest that RORa acts independently of RORgt in programming TH17 pathogenicity and identifies RORa as a safer and more selective therapeutic target for the treatment of TH17-mediated autoimmunity.

2020-10-29 | GSE160327 | GEO

The effect of 1-Oleoyl-lysophosphatidylethanolamine (LPE) on the RORgt activity in Th17 cells

Project description:Th17 cells are a helper cell subset of pro-inflammatory T cells, which have diverse functions ranging from neutrophilic-inflammatory responses against pathogens to driving a number of autoimmune diseases. Accumulating evidence indicates that specific cellular lipid metabolic pathways that include fatty acid or cholesterol play an essential role in regulating the differentiation and function of Th17 cells. However, what molecular mechanisms link lipid metabolism and RORgt function during Th17-cell differentiation? By using a combination of a CRISPR- based screening system and a global lipidome analysis, we addressed this question in an effort to identify a specific lipid metabolite that is essential for RORgt-mediated Th17-cell differentiation. We found five lipid enzymes that elicit RORgt activity and constitute a core molecular signature of Th17 cells. Furthermore, although Th17 cells treated with TOFA, which is a ACC1 inhibitor, showed decreased mRNA expression of Th17 specific gene and chromatin accessibility at Th17 cell specific gene loci, we also found that extrinsic supplementation of LPE (1-18:1) restored the phenotype of ACC1-inhibited Th17 cells. Taken together, these series of results indicated that LPE (1-18:1) synthesized from the five lipid metabolic enzymes was required for RORgt to function appropriately in Th17-cell differentiation.

2023-05-08 | GSE230624 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data