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Gene expression profiling in murine monocyte-dendritic cell progenitors (MDPs), common monocyte progenitors (cMoPs) and 32Dcl.3 cells transduced with C/EBPalpha and/or IRF8

ABSTRACT: To understand the mechanism by which IRF8 inhibits neutrophil differentiation

ORGANISM(S): Mus musculus

PROVIDER: GSE50052 | GEO | 2014/08/26

SECONDARY ACCESSION(S): PRJNA215873

REPOSITORIES: GEO

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Gene expression profiling in murine monocyte-dendritic cell progenitors (MDPs), common monocyte progenitors (cMoPs) and 32Dcl.3 cells transduced with C/EBPalpha and/or IRF8

Project description:To understand the mechanism by which IRF8 inhibits neutrophil differentiation Murine bone marrow MDPs and cMoPs were isolated by cell sorting from wild-type or Irf8 deficient mice. 32Dcl.3 cells were transduced with retroviruses carrying murine C/EBPalpha cDNA and/or murine Irf8 cDNA. Two independent experiments were performed.

2014-08-26 | E-GEOD-50052 | biostudies-arrayexpress

Whole transcriptome profiling of macrophage-DC progenitors (MDPs) and common monocyte progenitors (cMoPs) from Dnmt1+/+ and Dnmt1c/chip mice

Project description:Dendritic cells (DCs) are critical immune regulators involved in autoimmune diseases, but exploiting them clinically requires a detailed picture on the mechanisms orchestrating their development. DNA methylation is attractive in this regard because it is reversible and as such allows therapeutic manipulation. Combining single cell transplantation assays with whole-genome methylation assessment and with mice expressing reduced DNA methyltransferase 1 levels, we show that conventional and plasmacytoid DCs arise from myeloid-restricted hematopoietic stem cells (HSCs), suggesting that both subsets can develop independently of the lymphoid pathway. DC commitment by these HSCs requires an intrinsically high methylation threshold to establish expression of DC genes, particularly the Flt3 cytokine receptor. Reducing methylation depleted DCs and ameliorated systemic lupus erythematosus in mice. These studies shed novel light on the DC origin, show how lineage- and subset-specific methylation dynamics regulate DC fate and provide a potential rationale for targeting DCs in autoimmunity by hypomethylating agents.

2021-11-22 | GSE163295 | GEO

Gene expression analyses in IRF8-induced monocyte differentiation

Project description:To understand the differentiation program in monocyte/macrophage differentiation, we performed ChIP-seq for IRF8 and H3K4me1 together with gene expression profiling during IRF8-induced monocyte differentiation. Both promoter-proximal and -distal binding of IRF8 associated with induction of the genes especially those related to monocytes/macrophages and immunity. DNA motif analysis for cis-regulatory elements of indirect IRF8 target genes predicted KLF4, essential for Ly6C+ monocyte development, to be a downstream transcription factor regulating the indirect target gene expression. Introduction of KLF4 into an Irf8-/- myeloid progenitor cell line induced a subset of IRF8 target genes and partially induced monocyte/macrophage differentiation. Together, this study revealed the genome-wide behavior of IRF8 and the IRF8-KLF4 axis during monocyte differentiation. Gene expressions in monocyte-like cells differentiated by IRF8 or KLF4 were measured at day 4 after retroviral transductions to myeloid progenitor cell line, Tot2. Two independent experiments were performed.

2013-01-24 | E-GEOD-38810 | biostudies-arrayexpress

Methylomes of macrophage-DC progenitors (MDPs), monocytes, common monocyte progenitors (cMoPs), common dendritic cell progenitors (CDPs), plasmacytoid dendritic cells (pDCs), and cDC CD8a+ as well as cDC CD11b+ dendritic cells

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Gene expression analyses in IRF8-induced monocyte differentiation

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Regulation of an lncRNA irf8 by the Ikzf1/Myb complex drives neutrophil development

Project description:As critical executors of the immune system, neutrophils provide an immediate inflammatory response for the clearance of debris and microbes, which is essential for the protection of health. Developmentally, neutrophils and macrophages share common progenitors, whose fate is tightly controlled by transcriptional programs. Dysregulation of these programs causes severe hematological disorders, including neutropenia, neutrophilia, leukemia, and inflammatory disorders. However, the mechanisms underlying the generation of neutrophils through these programs are poorly understood. Here, we revealed that Ikzf1 and Myb were enriched in neutrophils. Overactivation of Ikzf1 promoted neutrophil generation while suppressing macrophage emergence. Conversely, the simultaneous loss of Ikzf1 and Myb, but not the individual mutations, drastically impaired neutrophil production and enlarged the macrophage pool in both zebrafish and mice. Mechanistically, Ikzf1 and Myb formed a complex that targeted irf8 and induced the expression of a long non-coding RNA (lncRNA), irf8-2, through a novel regulatory element. LncRNA irf8-2 biased neutrophil commitment by modulating irf8 dosage via Zfp36l1. The deletion of irf8-2 resulted in defective neutrophil development and enhanced macrophage production. However, a partial ratio of neutrophils and macrophages was restored when Ikzf1, Myb, and Irf8 were all compromised. Overall, our study reveals that Ikzf1 and Myb cooperatively bias neutrophil development against Irf8 via the lncRNA irf8-2 and Zfp36l. This study provides novel insights into the conserved molecular balance between neutrophil and macrophage development during myelopoiesis, with potential implications for understanding and treating myeloid disorders.

2025-09-24 | GSE306885 | GEO

Analysis of TF binding sites and histone modification in IRF8-induced monocyte differentiation

Project description:Chromatins were prepared from myeloid progenitor cell line Tot2 cells transduced with retrovirus for control MSCV or MSCV-IRF8. Chromatin immunoprecipitation (ChIP) was carried out by using anti-IRF8 antibody, anti-PU.1 antibody or anti-histone H3K4me1 antibody. ChIP-Seq peaks were identified using the FindPeaks tool in the HOMER package or SICER with input DNA tags as background distribution. Potential IRF8-direct target genes were identified based on ChIP-Seq and the alteration of expression by IRF8-induction. Examination of 2 transcription factor occupancy and 1 histone modifications in myeloid progenitor cells and monocyte-like cells differetiated by IRF8 expression

2013-01-24 | E-GEOD-38824 | biostudies-arrayexpress

Whole transcriptome profiling of macrophage-DC progenitors (MDPs) and common monocyte progenitors (cMoPs) from Dnmt1+/+ and Dnmt1c/chip mice

Project description:Whole transcriptome profiling of macrophage-DC progenitors (MDPs) and common monocyte progenitors (cMoPs) from Dnmt1+/+ and Dnmt1c/chip mice

| PRJNA685646 | ENA

Analysis of TF binding sites and histone modification in IRF8-induced monocyte differentiation

2013-01-24 | GSE38824 | GEO

Monocyte Subsets with High Osteoclastogenic Potential and Their Epigenetic Regulation Orchestrated by IRF8 [RNA-Seq]

Project description:Currently, it is unclear if all monocyte subsets exhibit osteoclastogenic potential. Furthermore, the role of lineage determining TFs in regulating OC differentiation on a genome-wide scale remains poorly understood. In this study, we utilized a novel Irf8 conditional knockout (Irf8 cKO) mouse model to characterize the importance of IRF8 in OC progenitor development and epigenetic regulation of OC differentiation. We performed RNA-seq on Irf8 gWT, gKO, cWT and cKO BMMs, preosteoclasts (PreOCs), and OCs. Cells were analyzed prior to (BMMs) and 3 days (PreOCs) and 6 days (OCs) after RANKL stimulation. Here we show that greater a number of genes are significantly upregulated in Irf8 cKO OCs when compared to WT and Irf8 gKO OCs. Altogether, our data shows that Irf8 cKO mice provide more precise/reliable OC-specific transcriptomic results when compared to Irf8 gKO mice.

2020-09-11 | GSE151388 | GEO

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