Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis reveals LZ-8 promotes the differentiation of Th17 cells [RNASeq2]

ABSTRACT: Transcriptome analysis reveals LZ-8 promotes the differentiation of Th17 cells [RNASeq2]

PROVIDER: PRJNA820610 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18500453.fastq.gz	Fastqsanger.gz
	SRR18500454.fastq.gz	Fastqsanger.gz
	SRR18500455.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

Transcriptome analysis reveals LZ-8 promotes the differentiation of Th17 cells [RNASeq2]

Project description:LZ-8 is an immunomodulatory protein derived from the large edible fungus Ganoderma lucidum. LZ-8 has therapeutic effects on several disorders of the immune system. T lymphocytes are considered to be one of the target cells of LZ-8. In order to comprehensively and systematically study the immunomodulatory effect of LZ-8 on T lymphocytes at the transcriptome level, we used RNA-seq technology to sequence the transcriptome of mouse T lymphocytes treated with LZ-8 for 10 hours and 0 hour. Differential gene analysis showed that 1275 genes were up-regulated and 2273 genes were down regulated after LZ-8 treatment for 10h. The pathway enrichment analysis showed that differential genes were enriched in terms of "Th1 and Th2 cell differentiation", "Th17 cell differentiation" and "IL-17 signaling pathway". RT-qPCR experiment confirmed that LZ-8 could upregulate the transcription level of Il4, Il13, Il17f and Csf2 in T lymphocytes, and the inhibitor Bay 11-7082 which inhibited NF κ B signaling pathway can reverse the transcriptional upregulation of Il2, Il17a and Irf4 by LZ-8. In conclusion, transcriptome sequencing data combined with RT-qPCR confirmed the promoting effect of LZ-8 on Th17 differentiation.

2025-03-28 | GSE199520 | GEO

Human Th17 Cell differentiation

Project description:The early stages of human Th17 Cell differentiation were studied using label free proteomics to compare Th17 polarized CD4+ human T cells at 24 h and 72 h with activated cells (72 and 24 h) and Thp cells.

2019-01-28 | PXD008973 | Pride

CCL20-CCR6 signaling alters the metabolic reprogramming to promote the pathogenic Th17 cell differentiation

Project description:Chemokine receptor CCR6 is a G-protein-coupled receptor that binds its high-affinity ligand, CCL20. Among the CD4+ T cells, Th17 and regulatory T cells express CCR6, which facilitates their migration in CCL20-enriched, inflamed tissue. Migration of CCR6+ T cells from secondary lymphoid tissues into inflamed tissues exposes them to a distinct metabolic microenvironment. What drives the metabolic adaptation of cells in these tissues and what contributes to their effector or regulatory function is not clearly understood. During colitis, increased gut production of CCL20 promotes the recruitment of these cells. We demonstrated that the intrinsic signaling of CCL20-CCR6 in CD4+ T cells promotes the differentiation of inflamatory Th1-like Th17 cells (T-bet+RORγt+) during colitis in both mouse models and humans. This signaling induces rapamycin-sensitive phosphorylation of PI3K, Akt, mTORC1, and STAT3 in a CCR6-dependent manner. RNA-seq and proteomics analysis revealed alterations in CCL20 during Th17 differentiation, affecting several metabolic pathways, including energy metabolism. CCL20 significantly increased glycolysis and inhibited oxidative phosphorylation, thereby driving the differentiation of pathogenic Th17 cells. Our findings suggest that alterations in CCR6-induced changes in Th17 metabolism offer an interesting therapeutic target for gut inflammation and autoimmunity.

2025-12-10 | PXD071790 | Pride

Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq2]

Project description:Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq2]

| PRJNA1299895 | ENA

Role of Stat3 phosphorylation in Th17 differentiation

Project description:Determine the role of stat3 phosphorylation, particularly at S727, during the differentiation of Th17 cells.

2025-10-29 | PXD059588 | Pride

Investigating the role of STAT3 in Th17 differentiation

Project description:Our lab is working to understand the role of STAT3 and the phosphorylation at S727 in Th17 cell differentiation

2025-10-29 | PXD065517 | Pride

ZEB1 Promotes Pathogenic Th1 and Th17 Cells Differentiation in Autoimmune Disease

Project description:ZEB1 Promotes Pathogenic Th1 and Th17 Cells Differentiation in Autoimmune Disease

| PRJNA745201 | ENA

CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

Protein arginine methyltransferase 5 promotes cholesterol biosynthesis mediated Th17 responses and autoimmunity [Th17]

Project description:Protein Arginine Methyltransferase (PRMT) 5 catalyzes symmetric dimethylation of arginine, a post-translational modification involved in cancer and embryonic development. However, the role and mechanisms by which PRMT5 modulates T helper (Th) cell polarization and autoimmune disease have not yet been elucidated. Here we find that PRMT5 promotes expression of cholesterol biosynthetic pathway enzymes that produce ROR agonists and activate ROR-t, driving Th17 differentiation. Specific loss of PRMT5 in the CD4 Th cell compartment completely protected mice from EAE. We also find that PRMT5 controls thymic and peripheral homeostasis in the CD4 Th cell life cycle, as well as iNK T and CD8 T cell development or maintenance, respectively. This work conclusively demonstrates that PRMT5 expression in recently activated T cells is necessary for expression of a cholesterol biosynthesis metabolic gene expression program that generates ROR-t agonistic activity and promotes Th17 differentiation and EAE. These results point to Th PRMT5 and its downstream cholesterol biosynthesis pathway as promising therapeutic targets in Th17-mediated diseases.

2020-02-27 | GSE141194 | GEO

Reconstruction of the dynamic regulatory network that controls Th17 cell differentiation by systematic perturbation in primary cells (Th17 differentiation timecourse)

Project description:Despite their enormous importance, the molecular circuits that control the differentiation of Th17 cells remain largely unknown. Recent studies have reconstructed regulatory networks in mammalian cells, but have focused on short-term responses and relied on perturbation approaches that cannot be applied to primary T cells. Here, we develop a systematic strategy – combining transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based tools for performing gene perturbations in primary T cells – to derive and experimentally validate a temporal model of the dynamic regulatory network that controls Th17 differentiation. The network is arranged into two self-reinforcing and mutually antagonistic modules that either suppress or promote Th17 differentiation. The two modules contain 12 novel regulators with no previous implication in Th17 differentiation, which may be essential to maintain the appropriate balance of Th17 and other CD4+ T cell subsets. Overall, our study identifies and validates 39 regulatory factors that are embedded within a comprehensive temporal network and identifies novel drug targets and organizational principles for the differentiation of Th17 cells. Time course microarray data for Th17 differentiation, including Th0 control

2013-03-07 | E-GEOD-43955 | biostudies-arrayexpress

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