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Single cell RNA sequencing reveals distinct clusters of Irf8 dependent pulmonary conventional dendritic cells

ABSTRACT: Single cell RNA sequencing reveals distinct clusters of Irf8 dependent pulmonary conventional dendritic cells

PROVIDER: PRJNA802572 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17846232.fastq.gz	Fastqsanger.gz
	SRR17846233.fastq.gz	Fastqsanger.gz
	SRR17846234.fastq.gz	Fastqsanger.gz
	SRR17846235.fastq.gz	Fastqsanger.gz
	SRR17846236.fastq.gz	Fastqsanger.gz

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Single cell RNA sequencing reveals distinct clusters of Irf8 dependent pulmonary conventional dendritic cells

Project description:We hereby report application of single cell RNA sequencing in order to understand heterogeneity within macrophages and conventional dendritic cells found in murine lungs. In this paper we specifically show different populations of cDCs as revealed through single cell RNA sequencing

2023-05-04 | GSE195899 | GEO

IRF8 transcription factor controls survival and function of terminally differentiated conventional and plasmacytoid dendritic cells respectively

Project description:Interferon regulatory factor-8 (IRF8) has been proposed to be essential for development of monocytes, plasmacytoid dendritic cells (pDCs) and type 1 conventional dendritic cells (cDC1s) and remains highly expressed in differentiated DCs. Transcription factors that are required to maintain the identity of terminally differentiated cells are designated “terminal selectors”. Using BM chimeras, conditional Irf8fl/fl mice and various promotors to target Cre recombinase to different stages of monocyte and DC development, we have identified IRF8 as a terminal selector of the cDC1 lineage controlling survival. In monocytes, IRF8 was necessary during early but not late development. Complete or late deletion of IRF8 had no effect on pDC development or survival but altered their phenotype and gene expression profile leading to increased T cell stimulatory function but decreased type 1 interferon production. Thus, IRF8 differentially controls the survival and function of terminally differentiated monocytes, cDC1s and pDCs.

2016-09-20 | GSE85520 | GEO

Gene expression data from mouse conventional dendritic cells (cDC) [IRF4,IRF8 DKO]

Project description:Gene expression data from mouse conventional dendritic cells (cDC) [IRF4,IRF8 DKO]

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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

The regulatory effect of IRF8 on the gene expression profiles of bone marrow derived dendritic cells

Project description:To investigate the role of IRF8 in the inflammatory microenvironment of abdominal aortic aneurysm tissue, bone marrow cells were isolated from the tibias and femurs of 8-week-old male mice and cultured with granulocyte-macrophage colony-stimulating factor and Flt3L cytokines to generate CD103-positive dendritic cells. Cells were harvested on days 9 and 15-16 and stimulated with tumor necrosis factor-alpha. Gene ontology analysis revealed upregulation of T cell activation and chemotaxis in bone marrow-derived dendritic cells from IRF8 overexpression mice, indicating IRF8's role in dendritic cell-T cell interactions. Protein-protein interaction analysis highlighted Cd40 and Fcgr1 as key surface markers. IRF8-related genes were enriched in type I interferon signaling pathways, implicating IRF8 in antigen presentation functions of dendritic cells.

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Gene expression data from mouse conventional dendritic cells (cDC) [IRF4,IRF8 DKO]

Project description:We used microarrays to detail cDC gene expression program controlled by IRF4 and IRF8.

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Optimization of the Irf8 +32 kb enhancer disrupts dendritic cell lineage segregation [scRNA-seq]

Project description:Autoactivation of lineage-determining transcription factors (TFs) mediates bistable expression to generate distinct cell phenotypes essential for complex body plans. Classical dendritic cells type 1 (cDC1) and type 2 (cDC2) provide non-redundant functions required for defense against distinct immune challenges. Interferon Regulatory Factor 8 (IRF8), the cDC1 lineage-determining TF, undergoes autoactivation in cDC1 progenitors to establish cDC1 identity, yet its expression is downregulated during cDC2 differentiation by an unknown mechanism. This study reveals that the Irf8 +32 kb enhancer, responsible for IRF8 autoactivation, has been tuned to possess low-affinity IRF8 binding sites. Incorporation of multiple high-affinity IRF8 binding sites into the Irf8 +32 kb enhancer induces erroneous IRF8 autoactivation in specified cDC2 progenitors, causing their redirection towards cDC1 and a novel hybrid DC subset with mixed lineage phenotypes. These developmental alterations critically impair both cDC1- and cDC2-dependent arms of immunity. Collectively, our findings underscore the significance of enhancer suboptimization in the developmental segregation of classical dendritic cells required for normal immune function.

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Inflammatory type 2 conventional dendritic cells contribute to murine and human cholangitis

Project description:Cholangitis mouse models were characterised by selective intrahepatic expansion of type 2 conventional dendritic cells, whereas plasmacytoid and type 1 conventional dendritic cells were not expanded. Expansion of type 2 conventional dendritic cells in human PSC lesions was confirmed by histology. Depletion studies revealed a pro-inflammatory role of type 2 conventional dendritic cells. Single-cell transcriptomics confirmed inflammatory maturation of the intrahepatic type 2 conventional dendritic cells and identified dendritic cell-derived inflammatory mediators.

2022-07-08 | E-MTAB-11821 | biostudies-arrayexpress

Optimization of the Irf8 +32 kb enhancer disrupts dendritic cell lineage segregation [bulk RNA-seq]

Project description:Autoactivation of lineage-determining transcription factors (TFs) mediates bistable expression to generate distinct cell phenotypes essential for complex body plans. Classical dendritic cells type 1 (cDC1) and type 2 (cDC2) provide non-redundant functions required for defense against distinct immune challenges. Interferon Regulatory Factor 8 (IRF8), the cDC1 lineage-determining TF, undergoes autoactivation in cDC1 progenitors to establish cDC1 identity, yet its expression is downregulated during cDC2 differentiation by an unknown mechanism. This study reveals that the Irf8 +32 kb enhancer, responsible for IRF8 autoactivation, has been tuned to possess low-affinity IRF8 binding sites. Increasing these affinities in vivo induces erroneous IRF8 autoactivation in specified cDC2 progenitors, causing their redirection towards cDC1 and a novel hybrid DC subset with mixed lineage phenotypes. These developmental alterations critically impair both cDC1- and cDC2-dependent arms of immunity. Collectively, our findings underscore the significance of enhancer suboptimization in the developmental segregation of classical dendritic cells required for normal immune function.

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