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ABSTRACT: Steroid-resistant gut graft-versus-host disease results from expansion of Th/Tc22, dysbiosis, and depletion of CX3CR1hi phagocytes

PROVIDER: PRJNA667464 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12775068_subreads.fastq.gz	Fastqsanger.gz
	SRR12775069_subreads.fastq.gz	Fastqsanger.gz
	SRR12775070_subreads.fastq.gz	Fastqsanger.gz
	SRR12775071_subreads.fastq.gz	Fastqsanger.gz
	SRR12775072_subreads.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 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 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

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

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

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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

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Loss of L-cells due to acute graft-versus-host disease leads to Paneth cell defects which can be compensated by glucagon like peptide-2

Project description:Paneth cells are targets of allo-reactive T cells during acute graft-versus-host disease (GVHD). GVHD-related loss of Paneth cells is connected to intestinal dysbiosis and a decline of antimicrobial peptides. Glucagon-like-peptide-2 (GLP-2) is an enteroendocrine tissue hormone, produced by the intestinal L-cells, that leads to expansion of Paneth cells. Microarray-based analysis of the intestinal tract revealed upregulation of a host-defense gene signature, increased Reg3-γ and Defensin-α-4 in the teduglutide treated group compared to the vehicle treated group. these results indicate that treatment of GVHD mice the GLP-2 analogue, teduglutide, restores intestinal homeostasis with increased Paneth cells and antimicrobial peptides

2023-10-29 | GSE138439 | GEO

FK506 and Lactobacillus acidophilus Ameliorate Acute Graft-Versus-Host Disease by Modulating the T Helper 17/Regulatory T-Cell Balance

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Project description:Oral Inflammation and Microbiome Dysbiosis Exacerbate Chronic Graft-versus-host Disease

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Project description:RATIONALE: Beclomethasone may be an effective treatment for graft-versus-host disease. PURPOSE: Phase I/II trial to study the effectiveness of beclomethasone in treating patients who have graft-versus-host disease of the esophagus, stomach, small intestine, or colon.

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