Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA379395 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5349710.fastq.gz | Fastqsanger.gz | |||
| SRR5349711.fastq.gz | Fastqsanger.gz | |||
| SRR5349712.fastq.gz | Fastqsanger.gz | |||
| SRR5349705.fastq.gz | Fastqsanger.gz | |||
| SRR5349706.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study was to to compare changes in chromatin status evoked by IFN-g signalling in Th9 cells. Furthermore, the binding of transcription factors IRF1 and IRF4 in Th9 cells were analysed to analyse whether IRF4 abundance is affected by IFN-g-induced IRF1 binding at regulatory regions in Th9 cells.
2017-03-17 | GSE96699 | GEO
Project description:Interferon regulatory factor 4 (IRF4) is an IRF family transcription factor with critical roles in lymphoid development and in regulating the immune response. IRF4 binds DNA weakly owing to a carboxy-terminal auto-inhibitory domain, but cooperative binding with factors such as PU.1 or SPIB in B cells increases binding affinity, allowing IRF4 to regulate genes containing ETS–IRF composite elements (EICEs; 5'-GGAAnnGAAA-3'). Here we show that in mouse CD4+ T cells, where PU.1/SPIB expression is low, and in B cells, where PU.1 is well expressed, IRF4 unexpectedly can cooperate with activator protein-1 (AP1) complexes to bind to AP1–IRF4 composite (5'-TGAnTCA/GAAA-3') motifs that we denote as AP1–IRF composite elements (AICEs). Moreover, BATF–JUN family protein complexes cooperate with IRF4 in binding to AICEs in pre-activated CD4+ T cells stimulated with IL-21 and in TH17 differentiated cells. Importantly, BATF binding was diminished in Irf4-/- T cells and IRF4 binding was diminished in Batf-/- T cells, consistent with functional cooperation between these factors. Moreover, we show that AP1 and IRF complexes cooperatively promote transcription of the Il10 gene, which is expressed in TH17 cells and potently regulated by IL-21. These findings reveal that IRF4 can signal via complexes containing ETS or AP1 motifs depending on the cellular context, thus indicating new approaches for modulating IRF4-dependent transcription. Genome-wide transcription factors mapping and binding of IRF4, BATF, IRF8, STAT3, JUN etc in WT, Irf4-/- and Batf-/- mice in different cell types (B cells, CD4+ T cells and TH17 cells) cultured with or without IL-21 was conducted. RNA-Seq is conducted in mouse B cells, CD4+ T cells, TH1/TH2/TH9/TH17/Treg.
2012-09-18 | E-GEOD-39756 | biostudies-arrayexpress
Project description:Compendium of high-throughput sequencing datasets derived from murine CD8+ T cells responding to infection, profiled by RNA-seq, ChIP-seq, and ATAC-seq at Naïve, Effector, and Memory timepoints across the Kaech, Goldrath, and Pereira labs, and ChIP-seq of various transcription factors across several labs Submission contains both original data from the Kaech lab and reanalysis of data from the Pereira and Goldrath labs, as well as various other labs corresponding to individual transcription factor ChIP-seq datasets, totaling to 96 reanalyzed GSM samples across several GSE series Included GSE series are: GSE95237 (Genome-wide maps of chromatin state and chromatin accessibility in CD8 T cell subsets), GSE95238 (Epigenetic landscapes reveal transcription factors that regulate CD8+ T cell differentiation), GSE88987 (Dynamic changes in chromatin accessibility in CD8+ T cells responding to viral infection), GSE58075 (Genome-wide mapping of Myc, AP4, and phosphorylated RNA polymerase II binding in activated CD8 T cells by ChIP sequencing), GSE54191 (ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells), GSE20898 (Genome-wide Analyses of Transcription Factor GATA3-Mediated Gene Regulation in Distinct T Cell Types), GSE46943 (Transcription Factor Foxo1 Controls Memory CD8+ T Cell Responses To Infection [ChIP-Seq]), GSE72997 (ChIP-Seq analysis of Helios and histone modifications in CD4+ and CD8+ Tregs), GSE50128 (Genome-wide maps of Runx3 bound regions in splenic IL-2-activated CD8+ T cells), GSE72565 (Binding of STAT5 upon IL-2 treatment to genomic sites in mouse CD8 T cells costimulated in vivo through CD134 plus CD137), GSE49930 (The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [ChIP-seq]), and GSE52070 (Genome-wide maps of Tcf1 binding locations in splenic CD8 T cells)
2018-03-17 | GSE111902 | GEO
Project description:Interleukin 9 (IL-9)-producing helper T (Th9) cells are essential for inducing anti-tumor immunity and inflammation in allergic and autoimmune diseases. Although transcription factors that are essential for Th9 cell differentiation have been identified, other signaling pathways that are required for their generation and functions are yet to be found. Here we identified that Epidermal Growth Factor Receptor (EGFR) is essential for IL-9 induction in Th cells. Moreover, amphiregulin (Areg), an EGFR ligand, is critical for the amplification of Th9 cells induced by TGF-β1 and IL-4. Furthermore, our data show that AREG-EGFR signaling induces HIF1α, which binds and transactivates IL-9, IRF4 and NOS2 promoters in Th9 cells. Loss of EGFR or HIF1α abrogates Th9 cell differentiation and suppress their anti-tumor functions. Moreover, in line with its reliance on HIF1α expression, metabolomics profiling of Th9 cells revealed that succinate, a TCA cycle metabolite, promotes Th9 cell differentiation and Th9 cell-mediated tumor regression.
2021-06-15 | GSE163056 | GEO
Project description:Interleukin 9 (IL-9) producing helper T (Th9) cells play a crucial role in allergic inflammation, autoimmunity, immunity to extracellular pathogens and anti-tumor immune response. In addition to Th9, Th2, Th17 and Foxp3+ Treg cells produce IL-9. Transcription factor that is critical for IL-9 induction in Th2, Th9 and Th17 cells has not been identified. Here we show that Foxo1, a forkhead family transcription factor, requires for IL-9 induction in Th9 and Th17 cells. We further show that inhibition of AKT enhances IL-9 induction in Th9 cells while it reciprocally regulates IL-9 and IL-17 in Th17 cells via Foxo1. Mechanistically, Foxo1 binds and transactivates IL-9 and IRF4 promoters in Th9, Th17 and iTregs. Furthermore, loss of Foxo1 attenuates IL-9 in mouse and human Th9 and Th17 cells, and ameliorates allergic inflammation in asthma. Our findings thus identify that Foxo1 is essential for IL-9 induction in Th9 and Th17 cells.
2017-07-09 | GSE100634 | GEO
Project description:The transcription factor IRF4 is crucial for the fate determination of pro-inflammatory T helper (Th)17 and the functionally opposing group of immunomodulatory regulatory T (Treg) cells. However, molecular mechanisms of how IRF4 steers diverse transcriptional programs in Th17 and Treg cells are far from being definitive. To unveil IRF4-driven lineage determination, we integrated data derived from affinity-purification and full mass spectrometry-based proteome analysis with chromatin immune precipitation sequencing. This allowed the characterization of subtype-specific molecular programs and the identification of IRF4 interactors in the Th17/Treg context. Our data reveal that IRF4-interacting transcription factors are recruited to IRF composite elements for the regulation of cell type-specific transcriptional programs as exemplarily demonstrated for FLI1, which in cooperation with IRF4 promotes Th17-specific gene expression. Inhibition of FLI1 markedly impaired Th17-differentiation. The present ‘omics’ dataset provides a valuable resource for studying IRF4-mediated gene regulatory programs in pro- and anti-inflammatory immune responses.
2025-03-05 | PXD060137 | JPOST Repository
Project description:we performed proteome analysis of Th9 cells to understand the involvement of proteins that might be crucial for the anti-tumor functions of Th9 cells. Here we show for the first time a comprehensive proteomic analysis of murine Th0 and Th9 cells, which identified 1451 total proteins among which 1367 proteins were common. Further analysis revealed that 118 proteins were upregulated while 81 proteins were downregulated in Th9 cells. Pathway analysis suggested an abundance of phosphoproteins in the proteome of Th9 cells. Among upregulated phosphoproteins which showed to be involved in immune 34 system, Ppp2ca (catalytic subunit of protein phosphatase, PP2A) was found to be highly expressed in Th9 cells. Although the role of PP2A has been shown to regulate the differentiation and functions of Th1,Th2, Th17 and Tregs, its role in differentiation and functions of Th9 cells is not identified yet. Our results show for the first time that PP2A is required for the differentiation and anti-tumor functions of Th9 cells. PP2A inhibition leads to the suppression of IL-9 induction and the expression of key transcription factors of Th9 cells.
2021-09-09 | PXD019506 | Pride
Project description:Genome-wide maps of chromatin state in liver.
| PRJNA636091 | ENA
Project description:Genome-wide maps of chromatin state in mTECs
| PRJNA433526 | ENA
Project description:Goal of this study was to compare transcriptional changes in IFN-gamma-treated WT compared to IRF1-deficient Th9 cells
2017-04-05 | GSE96818 | GEO