Transcriptional and Epigenetic analysis of IRF4-deficient B cell differentiation
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ABSTRACT:
PROVIDER: PRJNA725523 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14336500_1.fastq.gz | Fastqsanger.gz | |||
| SRR14336500_2.fastq.gz | Fastqsanger.gz | |||
| SRR14336600_1.fastq.gz | Fastqsanger.gz | |||
| SRR14336600_2.fastq.gz | Fastqsanger.gz | |||
| SRR14336501_1.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptional profiling of T-cells isolated from spleen of IRF4 -/- mice and cultured under Th17 polarizing conditions for 42 hrs compared to cells similarly isolated and cultured from spleen of IRF4 +/- mice. The aim of the study was to identify global misexpression of genes in IRF4 -/- cells and hence identify key pathways regulated by IRF4 during Th17 differentiation. Two-condition experiment, IRF4 -/- vs IRF4 +/- Th17 cells at 42hrs. Biological replicates: 3 for each condition
2012-09-13 | E-GEOD-40726 | biostudies-arrayexpress
Project description:Transcriptional profiling of T-cells isolated from spleen of IRF4 -/- mice and cultured under Th17 polarizing conditions for 42 hrs compared to cells similarly isolated and cultured from spleen of IRF4 +/- mice. The aim of the study was to identify global misexpression of genes in IRF4 -/- cells and hence identify key pathways regulated by IRF4 during Th17 differentiation.
2012-09-13 | GSE40726 | GEO
Project description:We analyzed the transcriptome differences of wild-type and IRF4-deficient (CD11c-cre x Irf4fl/fl) type-2 conventional dendritic cells (cDC2s) in spleen. Wild-type or IRF4-deficient (CD11c-cre x Irf4fl/fl) bone marrow cells were transferred into lethal irradiated CD45.1 mice. 8 weeks later, splenic cDC2s were purified and prepared for RNA-seq analysis. Three technical repeats of ~10^5 cells per sample from each of one mouse were included. CD97 was downregulated in IRF4-deficient cDC2s. GSEA showed that upregulated and downregulated genes in CD97-deficient cells were strongly enriched in IRF4-regulated genes. These data are in accord with CD97 acting within the IRF4 gene-expression network.
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Project description:To define molecular basis underlying dysfunction of Irf4-deficient T cells. We found that Irf4-deficient T cells were dysfunctional and unable to infiltrate and reject heart allografts, and then investigated the molecular basis underlying dysfunction of Irf4-deficient T cells. Irf4-deficient and wild type B6 CD4+ T cells were activated in vitro for two days, followed by microarray analysis. We found that dysfunction of Irf4-deficient T cells is not only due to impaired effector differentiation, but also involves an altered transcriptional programme that allows the expression of essential negative regulators of T-cell function.
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Project description:The aim of experiment was to study on genome-wide level IRF4 target genes in chicken DT40 B cell line, by comparizon of gene expression profiles of IRF4-deficient DT40 cells with WT IRF4 DT40 cells .
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Project description:FoxP3+ regulatory T (Treg) cells restrict excessive immune responses and immunopathology as well as reactivity to self or environmental antigens and thus are crucial for peripheral immune tolerance. The transcription factor Interferon Regulatory Factor 4 (IRF4) controls differentiation and function of T cells. In Treg cells, IRF4 is required for peripheral activation and maturation to effector Treg (eTreg) cells with enhanced suppressive function. However, the mechanisms of Treg cell regulation by IRF4 are not fully understood. Here, we analyze the role of IRF4 in differentiation and maintenance of Treg cells using IRF4-deficient mice and a T cell transfer model, that allows Irf4 inactivation in peripheral T cells. We demonstrate that loss of one Irf4 allele already results in impaired eTreg cell differentiation and decreased Treg cell homeostasis, indicating that IRF4 controls peripheral Treg cell differentiation in a dose dependent mode. Peripheral Irf4 inactivation was also associated with enhanced production of inflammatory but also inhibitory cytokines by Treg cells. ATAC sequencing of Treg cells after mutation of one or both Irf4 alleles revealed regions with altered accessibility in genes involved in Treg cell function. In the FoxP3 gene, Irf4 inactivation resulted in reduced ATAC signals in the promoter region and in the conserved non-coding sequence (CNS) 2, required for stability of FoxP3 expression in peripheral Treg cells in response to TCR stimulation. IRF4 deficient Treg cells also displayed a reduction in open chromatin in several Treg cell specific super enhancers, mainly located in proximity to potential IRF4 binding sites. In conclusion, our results demonstrate that IRF4 controls peripheral Treg cell differentiation and homeostasis in a dose dependent manner.
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Project description:To analyse the Irf4-dependent transcriptional changes of mouse bone marrow-derived macrophages (BMM) in response to IL-4, we have employed whole genome microarray expression profiling. For this purpose, bone marrow cells were isolated from 8 to 12 weeks old Irf4-deficient or heterozygous mice and cultured in the presence of the macrophage colony-stimulating factor (M-CSF) . After seven days of culture, IL-4 was added for 4 and 18 hours. Keywords: Mouse strain comparision; Gene expression profiling IL-4 induced gene expression was investigated in mouse bone marrow-derived macrophages (BMM) of Irf4-deficient or heterozygous mice. BMM were incubated with mouse recombinant IL-4 for 4 or 18 hours or without for 18 hours. Three independent experiments were performed at each time point (mock, 4 and 18 hours) using littermates for each experiment.
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Project description:Multiple myeloma (MM) is an incurable malignancy of plasma cells that exploits transcriptional networks driven by IRF4. To discover unique molecular vulnerabilities in MM centered on IRF4, we employ a multi-omics approach integrating functional genomics screening, spatial proteomics, and global chromatin mapping. We find that ARID1A, a member of the SWI/SNF chromatin remodeling complex, is both required for IRF4 expression and functionally associated with IRF4 protein on chromatin. Deletion of Arid1a in activated murine B cells thwarts subsequent plasma cell differentiation by disrupting IRF4-dependent transcriptional networks, therefore defining ARID1A as a novel plasma cell vulnerability. Targeting ARID1A-dependent SWI/SNF activity via SMARCA2/4 inhibition induces a rapid loss of IRF4-target gene expression and quenches global amplification of oncogenic gene expression driven by MYC, resulting in profound toxicity to MM cells. Notably, MM patients with aggressive disease have markers of SWI/SNF activity, and SMARCA2/4 inhibitors retain their activity in immunomodulatory drug (IMiD)-resistant MM cells. To fully harness the potential of these drugs, we use combinatorial drug screens to uncover profound synergistic toxicity between SMARCA2/4 and MEK inhibitors. Thus, targeting SWI/SNF activity potently represses an IRF4-MYC feed forward loop and provides a feasible path to effectively treat this incurable disease.
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Project description:Natural Killer (NK) cells are innate cytotoxic lymphocytes with adaptive immune features, including antigen-specificity, clonal expansion, and memory. As such, NK cells share many transcriptional and epigenetic programs with their adaptive CD8+ T cell siblings. Various signals ranging from antigen, co-stimulation, and proinflammatory cytokines are required for optimal NK cell responses in mice and humans during virus infection; however, the integration of these signals remains unclear. In this study, we identified the transcription factor IRF4 as a signal integrator to coordinate the NK cell response during viral infection. Loss of IRF4 was detrimental to the expansion and differentiation of virus-specific NK cells. This defect was partially attributed to the inability of IRF4-deficient NK cells to uptake nutrients required for survival and memory generation. Altogether, these data suggest IRF4 is a signal integrator that acts as a secondary metabolic checkpoint to orchestrate the adaptive response of NK cells during viral infection.
2023-08-03 | GSE235064 | GEO
Project description:Natural Killer (NK) cells are innate cytotoxic lymphocytes with adaptive immune features, including antigen-specificity, clonal expansion, and memory. As such, NK cells share many transcriptional and epigenetic programs with their adaptive CD8+ T cell siblings. Various signals ranging from antigen, co-stimulation, and proinflammatory cytokines are required for optimal NK cell responses in mice and humans during virus infection; however, the integration of these signals remains unclear. In this study, we identified the transcription factor IRF4 as a signal integrator to coordinate the NK cell response during viral infection. Loss of IRF4 was detrimental to the expansion and differentiation of virus-specific NK cells. This defect was partially attributed to the inability of IRF4-deficient NK cells to uptake nutrients required for survival and memory generation. Altogether, these data suggest IRF4 is a signal integrator that acts as a secondary metabolic checkpoint to orchestrate the adaptive response of NK cells during viral infection.
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