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Runx3 prevents spontaneous colitis by directing differentiation of anti-inflammatory mononuclear phagocytes

ABSTRACT: Runx3 prevents spontaneous colitis by directing differentiation of anti-inflammatory mononuclear phagocytes

PROVIDER: PRJNA561149 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10003833.fastq.gz	Fastqsanger.gz
	SRR10003834.fastq.gz	Fastqsanger.gz
	SRR10003835.fastq.gz	Fastqsanger.gz
	SRR10003836.fastq.gz	Fastqsanger.gz
	SRR10003837.fastq.gz	Fastqsanger.gz

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Runx3 prevents spontaneous colitis by directing the differentiation of anti-inflammatory mononuclear phagocytes.

Project description:Mice deficient in the transcription factor Runx3 develop a multitude of immune system defects, including early onset colitis. This paper demonstrates that Runx3 is expressed in colonic mononuclear phagocytes (MNP), including resident macrophages (RM) and dendritic cell subsets (cDC2). Runx3 deletion in MNP causes early onset colitis due to their impaired maturation. Mechanistically, the resulting MNP subset imbalance leads to up-regulation of pro-inflammatory genes as occurs in IL10R-deficient RM. In addition, RM and cDC2 display a marked decrease in expression of anti-inflammatory/TGF β-regulated genes and β-catenin signaling associated genes, respectively. MNP transcriptome and ChIP-seq data analysis suggest that a significant fraction of genes affected by Runx3 loss are direct Runx3 targets. Collectively, Runx3 imposes intestinal immune tolerance by regulating maturation of colonic anti-inflammatory MNP, befitting the identification of RUNX3 as a genome-wide associated risk gene for various immune-related diseases in humans, including gastrointestinal tract diseases such as Crohn's disease and celiac.

| S-EPMC7250423 | biostudies-literature

Runx3 prevents spontaneous colitis by directing differentiation of anti-inflammatory mononuclear phagocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-04 | GSE136067 | GEO

Runx3 function in colon resident macrophages (RM) and CD11b+ dendritic cells (DC).

Project description:RUNX3 is one of three mammalian Runt-domain transcription factors that regulate gene expression in several types of immune cells. Runx3-deficiency in mice is associated with a multitude of defects in the adaptive and innate immunity systems, including the development of early onset colitis. Our study reveals that conditional deletion of Runx3 specifically in mononuclear phagocytes (MNP) recapitulates the early onset spontaneous colitis seen in Runx3-/- mice. We show that Runx3 is expressed in colonic MNP, including RM and the dendritic cell cDC2 subsets and its loss results in impaired differentiation/maturation of both cell types. To uncover the immuno-tolerogenic properties of Runx3 in the colon MNP we performed global transcriptional profiling employing microarrays.

2020-06-04 | GSE136066 | GEO

cecum mononuclear phagocytes

Project description:scRNAseq of cecum mononuclear phagocytes of PBS/LPS-treated mice

| PRJEB46461 | ENA

ImmGen ULI: OpenSource Mononuclear Phagocytes Project

Project description:Primary RNASeq data for progenitor, resident, and stimulated (C.alb, LPS, injury, APAP+ starved overnight and pIC) mononuclear phagocytes from fourteen organs.

2018-11-03 | GSE122108 | GEO

Mononuclear phagocytes in neonatal Peyer's patches

Project description:Mononuclear phagocytes in neonatal Peyer's patches

| PRJNA779989 | ENA

ImmGen ULI: OpenSource Mononuclear Phagocytes Project

Project description:ImmGen ULI: OpenSource Mononuclear Phagocytes Project

| PRJNA503607 | ENA

The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

2019-11-12 | PXD007511 | Pride

Identification of Fcmr-dependent heterogeneity in tumor associated mononuclear phagocytes

Project description:The mononuclear phagocytic system (MPS) is characterized by functional diversity and plasticity, including within the tumor microenvironment (TME). Tumor-associated mononuclear phagocytes (TMPs) within the TME come from various ontological origins. To determine how Fcmr deficiency might impact the functional heterogeneity of mature mononuclear phagocytes (MPs) within the TME, we performed single-cell RNA sequencing (scRNAseq) on MPs isolated from B16 tumors resected from Fcmr-/- and Fcmr+/+ mice. To evaluate a homogenous population of MPs within the TME we chose to examine cells harboring expression of markers found in more mature, differentiated MPs. Therefore, we then sorted MerTk+ CD64+ TMPs by FACS and subjected these cells to single-cell transcriptomic analyses using the Chromium 10X Genomics platform. We obtained RNAseq profiles from 6352 Fcmr+/+ and 7999 Fcmr-/- TMPs.

2019-06-18 | GSE130287 | GEO

MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice.

Project description:Commensal bacterial sensing by Toll-like receptors is critical for maintaining intestinal homeostasis, but can lead to colitis in the absence of interleukin-10. Although Toll-like receptors are expressed in multiple cell types in the colon, the cell type(s) responsible for the development of colitis are currently unknown. Here we generated mice that are selectively deficient in MyD88 in various cellular compartments in an interleukin-10(-/-) setting. Although epithelial expression of MyD88 was dispensable, MyD88 expression in the mononuclear phagocyte compartment was required for colitis development. Specifically, phenotypically distinct populations of colonic mononuclear phagocytes expressed high levels of interleukin-1?, interleukin-23 and interleukin-6, and promoted T-helper 17 responses in the absence of interleukin-10. Thus, gut bacterial sensing through MyD88 in mononuclear phagocytes drives inflammatory bowel disease when unopposed by interleukin-10.

| S-EPMC3521499 | biostudies-literature

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