Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of Ikaros in the transcriptional signature of Th17 cells

ABSTRACT: We found that CD4+ T cells require Ikaros to promote IL-17 production when cultured in Th17 conditions. To understand why Ikaros null T cells do not produce IL-17, we analyzed the transcriptome of WT vs. Ikaros null naive CD4+ T cells both resting (day 0) or activated with anti-CD3 plus anti-CD28 antibodies, IL-6, TGFb1 and neutralizing anti-IFNg and anti-IL-4 antibodies (Th17 condition) for 1 or 2 days. Samples from 3 independent experiments were analyzed.

ORGANISM(S): Mus musculus

PROVIDER: GSE133878 | GEO | 2021/04/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-SEQ analysis of CD4+ T cells in presence or absence of Ikaros.

Project description:We found by microarray analysis that Ikaros is critical to limit the expression of several pro-inflammatory genes during Th17 cell polarization. To unravel the role of Ikaros in the expression of pro-inflammatory genes without Th17 polarizing cytokines, we performed an RNA-seq analysis in naive CD4+ T cells and CD4+ T cells activated with anti-CD3+anti-CD28 antibodies (Th0 condition), from WT (Ikaros f/f CD4-Cre-) and Ikaros TKO mice (Ikaros f/f CD4-Cre+).

2021-04-26 | GSE157810 | GEO

Genome wide chromatin accessibility (ATAC-SEQ) in the presence or absence of Ikaros in CD4+ T cells.

Project description:We found that Ikaros is critical to limit the expression of pro-inflammatory cytokines in TCR/CD28-activated CD4+ T cells. To understand if Ikaros could modify the chromatin accessibility in regions controling the expression of these pro-inflammatory genes, we examined the chromatin state in naive CD4+ T cells and CD4+ T cells activated with anti-CD3+anti-CD28 antibodies for 1 and 2 days, from WT (Ikaros f/f CD4-Cre-) and Ikaros TKO mice (Ikaros f/f CD4-Cre+), using the ATAC-seq approach.

2021-04-26 | GSE157812 | GEO

Identification of genes controlled by Ikaros and IL-7 in the mouse Ikaros-deficient pre-B cell line BH1

Project description:The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1

2013-11-30 | GSE51350 | GEO

Identification of genes controlled by Ikaros and IL-7 in the mouse Ikaros-deficient pre-B cell line BH1

Project description:The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1

2013-11-30 | GSE51350 | GEO

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

Identification of genes controlled by Ikaros and IL-7 in the mouse Ikaros-deficient pre-B cell line BH1

Project description:The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1 The mouse BH1 pre-B cell line was transduced with retroviruses encoding Bcl2 and an Ikaros-estrogen receptor fusion protein. Doubly transduced cells were purified by FACS (BH1-Bcl2-Ik1ER). The transcriptome of these cells was analyzed at time 0, and after 6h and 24h of induction of Ikaros activity with 4-hydroxytamoxifen (4OHT) and/or withdrawal of IL-7. Samples from 2 independent experiments were analyzed (exp1 and exp2).

2013-11-30 | E-GEOD-51350 | biostudies-arrayexpress

G-Protein-Coupled Receptor 68 Negatively Regulates IL-22 Production in Human Th17 Cells

Project description:Purpose: To identify novel genes regulated by the aryl hydrocarbon receptor that influence human Th17 cell function. Methods: Naïve CD4 T cells from peripheral blood of six healthy human volunteers were cultured under four experimental conditions for three days: anti-CD3 and anti-CD28 antibodies (Media control), Media with Th17 conditions (IL-6, TGF-b, IL-1b, IL-23), Th17+FICZ and Th17+CH223191. Total RNA was extracted from each sample on day 3 and sequenced in a paired-end 2x50bp strategy on an Illumina HiSeq1500. A total of six donors were analyzed. Results: AhR activation with FICZ suppressed IL-17 production from human CD4 T cells and increased IL-22. AhR inhibition with CH223191 potently suppressed IL-22 and modestly increased IL-17 production. On day 3, the number of significantly regulated genes for each treatment were 975 (Th17), 88 (Th17+FICZ) and 142 (Th17+CH223191). 11 common genes were significantly regulated by all three treatments. One of these, GPR68, was investigated further in functional studies since its expression correlated with IL-22 production. Activation of GPR68 with a positive allosteric modulator suppressed IL-22 concentrations in human Th17 cell cultures. Conclusions: Our study demonstrates that GPR68 activation can negatively regulate IL-22 production from human CD4 T cells in the presence of an AhR agonist. RNA-seq is a powerful method to identify novel gene targets that regulate cytokines involved in chronic inflammatory diseases.

2018-07-19 | GSE102045 | GEO

Genome-wide binding of Ikaros in naive CD4+ T cells and Th0 at day1

Project description:The aim of the project is to determine the binding sites of Ikaros in CD4+ T cells. To perform this, CD4 naive T cells (CD4 TN; d0) either rested or activated with anti-CD3+anti-CD28 Abs for 1 day (Th0 d1) were subjected to a ChIP using anti-Ikaros Ab followed by high throughput sequencing.

2021-04-26 | GSE157811 | GEO

Ikaros-induced gene expression chages upon Ikaros re-expression in the ILC87 Ikaros-deficient tumor cell line

Project description:We used microarrays to analyze gene expression changes in the Ikaros null ILC87 T cell tumor line after re-expression of Ikaros.

2015-11-03 | GSE72801 | GEO

Transcriptional signature of human pro-inflammatory TH17 cells [ex vivo TH17 cells]

Project description:Human peripheral blood IFN-γ+IL-17+ (TH1/17) and IFN-γ–IL-17+ (TH17) CD4+ T cells display distinct transcriptional profiles in high-throughput transcription analyses. Compared to TH17 cells, TH1/17 cells have similar gene signatures to mouse pathogenic TH17 cells.

2017-09-29 | GSE104021 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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