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Granzyme A-producing CD4+ T cells in graft-versus-host disease

ABSTRACT: Granzyme A-producing CD4+ T cells in graft-versus-host disease

PROVIDER: PRJNA646973 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12252233_1.fastq.gz	Fastqsanger.gz
	SRR12252233_2.fastq.gz	Fastqsanger.gz
	SRR12252234_1.fastq.gz	Fastqsanger.gz
	SRR12252234_2.fastq.gz	Fastqsanger.gz
	SRR12252235_1.fastq.gz	Fastqsanger.gz

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Granzyme A-producing CD4+ T cells in 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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Somatic Gain-of-Function mTOR mutation in Clonally Expanded T-lymphocytes Associated with Chronic Graft-Versus-Host Disease

Project description:Graft-versus-host-disease (GvHD) is the main complication of allogeneic hematopoietic stem cell transplantation (HSCT). Here we report studies of a patient with chronic GVHD (cGVHD) carrying persistent CD4+ T cell clonal expansion which harbored somatic mTOR, NFKB2, and TLR2 mutations. Functional analysis of the discovered mTOR mutation indicated a gain-of-function alteration and activation of both mTORC1 and mTORC2 signaling pathways leading to increased cell proliferation and decreased apoptosis. Single-cell RNA sequencing and real-time impedance measurements supported increased cytotoxicity of mutated CD4+ T cells. High throughput drug-sensitivity testing suggested mutations induce resistance to mTOR inhibitors but increase sensitivity for HSP90 inhibitors. Our findings suggest that somatic mutations may contribute to aberrant T cell proliferations and participate in the persistent immune activation in cGVHD paving the way for novel targeted therapies.

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Transcriptome analysis of acute graft-versus-host disease in children

Project description:Transcriptome analysis of acute graft-versus-host disease in children

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Acute graft-versus-host disease (gene expression profiling)

Project description:Allogeneic hematopoietic stem cell transplantation (HSCT) is the treatment of choice for high-risk hematological malignancies, yet a major complication associated with this therapy is acute graft-versus-host disease (GVHD). Despite a well-defined pathophysiological mechanism, there are no definitive markers for predicting acute GVHD development or progression to advanced stages. In the current study, we enrolled four acute GVHD and four acute GVHD-free recipients of allogeneic HSCT and collected peripheral blood just prior to onset of clinical acute GVHD for analysis on Affymetrix GeneChip Human Genome U133 Plus 2.0 microarrays. We noted significant differences in expression of 1,658 genes between control and acute GVHD patients, based on an analysis of covariance (ANCOVA) by type of transplant, a pooled error estimate, and a false discovery rate (FDR) of 10%. In conclusion, we offer the first report of a preliminary molecular signature of acute GVHD in allogeneic HSCT patients.

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

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 cells but expansion of IL-17-IL-22+ Th/Tc22, particularly Tc22 cells. The IL-22 from Th/Tc22 cells causes dysbiosis.

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