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IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice II

ABSTRACT: IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice II

PROVIDER: PRJNA668828 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12816200_1.fastq.gz	Fastqsanger.gz
	SRR12816200_2.fastq.gz	Fastqsanger.gz
	SRR12816201_1.fastq.gz	Fastqsanger.gz
	SRR12816201_2.fastq.gz	Fastqsanger.gz
	SRR12816202_1.fastq.gz	Fastqsanger.gz

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IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice

Project description:IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice

| PRJNA668824 | ENA

IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice II

2020-12-27 | GSE159418 | GEO

IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice I

Project description:IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice I

| PRJNA667450 | ENA

IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice I

Project description:CD4+ and CD8+ T cells can reciprocally differentiate into Th/Tc1, Th/Tc17 and Th/Tc22. Although alloreactive Th/Tc1 cells play a critical role in initiating pathogenesis of gut acute graft-versus-host disease (Gut-aGVHD), the pathogenic T cells in steroid-resistant Gut-aGVHD (SR-Gut-aGVHD) remains unclear. Here, we show that in murine models of SR-Gut-aGVHD, the pathogenesis is associated with reduction of IFN-g+ Th/Tc1 and IL-17A+IL-22- Th/Tc17 but expansion of IL-17-IL-22+ Th/Tc22, particularly Tc22 cells. IL-22 from Th/Tc22 cells causes dysbiosis. Using a Gut-aGVHD model induced by alloreactive IFN-g-/- CD8+ T cells, we show that the Gut-aGVHD pathogenesis requires both dysbiosis and depletion of CX3CR1hi mononuclear phagocytes (MNP) that regulate intestinal bacterial translocation. Absence of IFN-g leads to preferential expansion of Tc22 that induce dysbiosis by augmenting RegIIIg production, and depletion of CX3CR1hi MNP via its PD-1 interaction with tissue PD-L1. Interestingly, SR-Gut-aGVHD is also associated with depletion of CX3CR1hi MNP that reduces expansion of Tc22 under steroid treatment. Our studies indicate that expansion of Th/Tc22, dysbiosis, and depletion of CX3CR1hi MNP cells play critical roles in SR-Gut-aGVHD pathogenesis. These results provide new avenue towards studies in patients and call for caution in clinical testing of IL-22 agonists or IFN-g antagonist in patients.

2020-12-27 | GSE159031 | GEO

IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice.

Project description:Efforts to improve the prognosis of steroid-resistant gut acute graft-versus-host-disease (SR-Gut-aGVHD) have suffered from poor understanding of its pathogenesis. Here we show that the pathogenesis of SR-Gut-aGVHD is associated with reduction of IFN-γ+ Th/Tc1 cells and preferential expansion of IL-17-IL-22+ Th/Tc22 cells. The IL-22 from Th/Tc22 cells causes dysbiosis in a Reg3γ-dependent manner. Transplantation of IFN-γ-deficient donor CD8+ T cells in the absence of CD4+ T cells produces a phenocopy of SR-Gut-aGVHD. IFN-γ deficiency in donor CD8+ T cells also leads to a PD-1-dependent depletion of intestinal protective CX3CR1hi mononuclear phagocytes (MNP), which also augments expansion of Tc22 cells. Supporting the dual regulation, simultaneous dysbiosis induction and depletion of CX3CR1hi MNP results in full-blown Gut-aGVHD. Our results thus provide insights into SR-Gut-aGVHD pathogenesis and suggest the potential efficacy of IL-22 antagonists and IFN-γ agonists in SR-Gut-aGVHD therapy.

| S-EPMC7865028 | biostudies-literature

IL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice

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

2020-12-27 | GSE159419 | GEO

Murine mononuclear phagocyte lineage cells

Project description:Murine mononuclear phagocyte lineage cells

| PRJNA630056 | ENA

Mononuclear phagocyte phenotypes in a multiple sclerosis model

Project description:Mononuclear phagocytes are key regulators of both tissue damage and repair in neuroinflammatory conditions such as multiple sclerosis (MS). To examine divergent phagocyte phenotypes in the inflamed central nervous system (CNS) we introduce an in vivo imaging approach combined with RNAseq and proteomics that allows us to temporally and spatially resolve the evolution of phagocyte polarization in a murine MS model. We show that the initial pro-inflammatory polarization of phagocytes is established after spinal cord entry and critically depends on the compartment they enter. Guided by signals from the CNS environment individual phagocytes then switch their phenotype as lesions move from expansion to resolution. Our study thus provides a first real-time analysis of the temporo-spatial determinants and regulatory principles of phagocyte specification in the inflamed CNS.

2019-07-10 | PXD010245 | Pride

Single-cell RNA profiling of mononuclear phagocyte in colorectal cancer

Project description:During mononuclear phagocyte system evolution, monocytes differentiate into pro-tumorigenic TAMs. We used single cell RNA sequencing (scRNA-seq) to analyze the characteristics of mononuclear phagocyte in colorectal cancer

2023-07-01 | GSE217774 | GEO

Gene expression data from Peyer's patch mononuclear phagocyte system

Project description:PeyerM-bM-^@M-^Ys patches (PP) are primary inductive sites of mucosal immunity. Defining PP mononuclear phagocyte system (MPS) is thus crucial to understand the initiation of mucosal immune response. We provide a comprehensive analysis of the phenotype, distribution, ontogeny, lifespan, function and transcriptional profile of PP MPS. We show that monocytes give rise to macrophages and to lysozyme-expressing DC (LysoDC) which are both involved in particulate antigen uptake, display strong innate antiviral and antibacterial gene signatures and, upon TLR7 stimulation, secrete IL-6 and TNF but no IL-10. However, unlike macrophages, LysoDC display a rapid renewal rate, strongly express genes of the MHCII presentation pathway and prime naM-CM-/ve helper T cells for IFNg production. Our results show that in PP, at steady state, monocytes generate both LysoDC and macrophages which display distinct features from their adjacent villus counterparts. 3 replicates of 3 different mononuclear phagocyte subsets have been extracted from Peyer's Patches of WT C57Bl/6 mice: CD11b+ DC, lysoDC and lysoMac. The total RNA of PP-sorted cells from the 3 independent experiments was extracted with a Qiagen micro RNAeasy PLUS kit. Quantity, quality and absence of genomic DNA contamination were assessed with a Bioanalyser (Agilent). Microarray experiments were performed by the Plateforme Biopuces of Strasbourg (France) using the GeneChipM-BM-. Mouse Gene 1.0 ST array.

2015-02-03 | E-GEOD-65514 | biostudies-arrayexpress

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