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Expression data from cDC2 derived from in vitro culture from Batf3 KO pre-cDC1 and IRF8 +32 KO pre-cDC1 compared to cDC1 derived from in vitro culture of WT pre-cDC1 or cDC2 derived from in vitro culture of WT pre-cDC2

ABSTRACT: We used gene expression microarrays to determine if Batf3 and the IRF8 +32 kb enhancer are required to sustain IRF8 expression in the pre-cDC1.

ORGANISM(S): Mus musculus

PROVIDER: GSE132768 | GEO | 2019/06/23

REPOSITORIES: GEO

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Expression data from cDC2 derived from in vitro culture from Batf3 KO pre-cDC1 and IRF8 +32 KO pre-cDC1 compared to cDC1 derived from in vitro culture of WT pre-cDC1 or cDC2 derived from in vitro culture of WT pre-cDC2

Project description:Expression data from cDC2 derived from in vitro culture from Batf3 KO pre-cDC1 and IRF8 +32 KO pre-cDC1 compared to cDC1 derived from in vitro culture of WT pre-cDC1 or cDC2 derived from in vitro culture of WT pre-cDC2

| PRJNA548946 | ENA

Irf8 deficiency induces functional, transcriptional and epigenetic reprogramming of cDC1 into the cDC2 lineage

Project description:Conventional dendritic cells (cDC) consist of two functionally and phenotypically distinct subsets, cDC1 and cDC2, whose development is dependent on distinct sets of transcription factors. Interferon regulatory factor 8 (IRF8) is required at multiple stages of cDC1 development, but its role in mature cDC1 remains unclear. Here we used XCR1-cre to delete Irf8 in committed cDC1 and demonstrate that Irf8 is required for maintaining the identify of cDC1 but not their survival. In the absence of Irf8, committed cDC1 (“ex-cDC1”) acquired the transcriptional, functional and chromatin accessibility properties of cDC2. This conversion was independent on Irf4 and was associated with decreased accessibility in putative IRF8, Batf3 and composite AP-1-IRF (AICE) binding elements, together with increased accessibility of cDC2 associated transcription factor binding elements. Thus, IRF8 expression by committed cDC1 is required for preventing their conversion into cDC2.

2022-06-21 | GSE168477 | GEO

RNA-seq analysis of mouse cDC1 and cDC2 populations upon DC-SCRIPT depletion

Project description:The functional diversification of dendritic cells (DCs) is a key step in establishing protective immune responses. Despite the importance of this lineage diversity, its genetic basis is not fully understood. DC-SCRIPT (Zfp366) is a poorly known transcription factor expressed in conventional DCs (cDCs) and their committed bone marrow progenitors but not in plasmacytoid DCs (pDCs). We show that mice lacking DC-SCRIPT displayed substantially impaired development of IRF8-dependent conventional DC1 (cDC1), while cDC2 differentiated normally. The residual DC-SCRIPT-deficient cDC1s had impaired CD8+ T-cell cross-priming, which could be in part explained by the direct control of DC-SCRIPT on IL-12p40 production. Genome-wide mapping of DC-SCRIPT binding and gene expression analyses revealed a key role for DC-SCRIPT in maintaining cDC1 identity via the direct regulation of cDC1 signature genes, including Irf8. Our study reveals DC-SCRIPT to be a critical component of the gene regulatory program shaping the functional attributes of cDC1s.

2021-02-24 | GSE165125 | GEO

DC-SCRIPT (Zpf366) binding in cDC1 and cDC2 cells from wildtype and DC-SCRIPT knockout mice

2021-02-24 | GSE165138 | GEO

RNA-seq and CUT&Tag analysis of mouse cDC1 and cDC2 populations upon DC-SCRIPT depletion

2021-02-24 | GSE165361 | GEO

Batf3 maintains Irf8 autoactivation for commitment of a novel clonogenic progenitor of CD8+DCs

Project description:The transcription factors Batf3 and IRF8 are required for development of CD8α+ conventional dendritic cells (cDCs), but the basis for their actions was unclear. Here, we identify two novel Zbtb46+ progenitors that separately generate CD8α+ and CD4+ cDCs and arise directly from the common DC progenitor (CDP). Irf8 expression in the CDP depends on prior PU.1-dependent autoactivation, and specification of pre-CD8 DC progenitors requires IRF8 but not Batf3. However, upon pre-CD8 DC specification, Irf8 autoactivation becomes Batf3-dependent at a CD8α+ cDC-specific enhancer containing multiple AP1-IRF composite elements (AICEs) within the Irf8 superenhancer. CDPs from Batf3-/- mice that specify toward pre-CD8 DCs fail to complete CD8α+ cDC development due to decay of Irf8 autoactivation, and divert to the CD4+ cDC lineage. Examination of histone modifications (H3K27ac and H3K4me1) and 2 transcription factors (Batf3 and Irf8) and the p300 co-factor binding in 3 different dendritic cell subsets

2015-06-08 | E-GEOD-66899 | biostudies-arrayexpress

Bulk RNA-seq of adult steady-state CD169+ metallophilic marginal zone macrophages and conventional dendritic cells type 1 sorted by flow cytometry from the spleen of adult BATF3 WT and BATF3 KO mice

Project description: Not available

| S-BSST950 | biostudies-other

Expression data from splenic cDC1, cDC2, and pDC from WT and Bcl6cKO mice

Project description:We used microarray gene analysis to compare the transcriptional profiles between WT and Bcl6cKO splenic cDC1, cDC2, and pDCs.

2019-10-01 | GSE135904 | GEO

Cis-regulation between Irf8 enhancers during cDC1 development (ATAC-Seq)

Project description:Type 1 classical dendritic cells (cDC1s) development requires the transcription factor IRF8, and IRF8 mutations cause severe combined immunodeficiency, including disseminated bacille Calmette-Guérin (BCG) disease. IRF8 regulated enhancers are required for Irf8 expression in early DC progenitors and mature cDC1s. The E-protein-dependent +41 kb enhancer gains accessibility and activates transcription in common DC progenitors (CDPs), and its depletion abrogated pre-cDC1s specification. The Batf3-dependent +32 kb enhancer gains accessibility and activates transcription in pre-cDC1 progenitors, and its depletion impaired cDC1 maturation. The +32 kb Irf8 enhancer locus bears an enhancer transcript, and the production of enhancer RNA (eRNA) Gm39266 is dependent on +41 kb Irf8 enhancer. It was unclear whether the +32 kb and +41 kb enhancers act independently or cooperate to regulate Irf8 expression. We dissected the mechanisms using +32/+41 compound heterozygous mice, and found that while the +41 kb enhancer suffices for pre-cDC1 progenitor specification, the +32 kb and +41 kb enhancers must reside on one allele to support cDC1 maturation. The +41 kb enhancer cis-regulates chromatin accessibility and BATF3 binding at +32 kb enhancer, independent of eRNA Gm39266 transcripts or transcription across +32 kb Irf8 enhancer.

2023-03-15 | GSE218990 | GEO

Cis-regulation between Irf8 enhancers during cDC1 development (CUT&RUN)

2023-03-15 | GSE218991 | GEO

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