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Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation [RNA-seq]

ABSTRACT: Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation [RNA-seq]

PROVIDER: PRJNA805294 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17979000_1.fastq.gz	Fastqsanger.gz
	SRR17979000_2.fastq.gz	Fastqsanger.gz
	SRR17979001_1.fastq.gz	Fastqsanger.gz
	SRR17979001_2.fastq.gz	Fastqsanger.gz
	SRR17979002_1.fastq.gz	Fastqsanger.gz

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Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation [WGBS]

Project description:Donor T-cell methylation state has an effect on alloreactivity. We applied WGBS and the InformME analysis pipeline to investigate the role of DNA methylation in mice receiving transplantation from T-cell conditional DNMT3a KO donors.

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Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation [RNA-seq]

Project description:Donor T-cell RNA expression state has an effect on alloreactivity. We applied RNA-Seq and the Deseq2 analysis pipeline to investigate the role of gene expression in mice receiving transplantation from T-cell conditional DNMT3a KO donors.

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Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation.

Project description:Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation.

| PRJNA805291 | ENA

Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation [WGBS]

Project description:Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation [WGBS]

| PRJNA805295 | ENA

Donor T cell DNMT3a regulates alloreactivity in mouse models of hematopoietic stem cell transplantation.

Project description:DNA methyltransferase 3a (DNMT3a) is an important part of the epigenetic machinery that stabilizes patterns of activated T cell responses. We hypothesized that donor T cell DNMT3a regulates alloreactivity after allogeneic blood and marrow transplantation (allo-BMT). T cell conditional Dnmt3a KO mice were used as donors in allo-BMT models. Mice receiving allo-BMT from KO donors developed severe acute graft-versus-host disease (aGVHD), with increases in inflammatory cytokine levels and organ histopathology scores. KO T cells migrated and proliferated in secondary lymphoid organs earlier and demonstrated an advantage in trafficking to the small intestine. Donor T cell subsets were purified after BMT for whole-genome bisulfite sequencing (WGBS) and RNA-Seq. KO T cells had global methylation similar to that of WT cells, with distinct, localized areas of hypomethylation. Using a highly sensitive computational method, we produced a comprehensive profile of the altered epigenome landscape. Hypomethylation corresponded with changes in gene expression in several pathways of T cell signaling and differentiation. Additionally, Dnmt3a-KO T cells resulted in superior graft-versus-tumor activity. Our findings demonstrate a critical role for DNMT3a in regulating T cell alloreactivity and reveal pathways that control T cell tolerance. These results also provide a platform for deciphering clinical data that associate donor DNMT3a mutations with increased GVHD, decreased relapse, and improved survival.

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Liver tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation.

Project description:To determine the circRNA expression profile in hepar tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation, we uesed circRNA microArray analysis form Arraystar to examine the expression of circRNAs and circRNAs in hepar tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation.

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Donor Macrophages Modulate Rejection after Heart Transplantation

Project description:Cellular rejection after heart transplantation imparts significant morbidity and mortality. Current immunosuppressive strategies are imperfect, target recipient T-cells, and have adverse effects. The innate immune response plays an essential role in the recruitment and activation of T-cells. Targeting the donor innate immune response would represent the earliest interventional opportunity within the immune response cascade. There is limited knowledge regarding donor immune cell types and functions in the setting of cardiac transplantation and no current therapeutics exist for targeting these cell populations. Distinct populations of donor and recipient macrophages co-exist within the transplanted heart. Donor CCR2+ macrophages are key mediators of allograft rejection and deletion of MYD88 signaling in donor macrophages is sufficient to suppress rejection and extend allograft survival. This highlights the therapeutic potential of donor heart-based interventions.

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Donor T-cell DNMT3a regulates alloreactivity in murine models of hematopoietic stem cell transplantation.

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

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Galectin-3 expression in donor T cells reduces GvHD severity and lethality after allogeneic hematopoietic cell transplantation

Project description:Abundant donor cytotoxic T cells that attack normal host organs remain a major problem for patients receiving allogeneic hematopoietic cell transplantation (Allo-HCT). Despite an increase in our knowledge of the pathobiology of acute graft versus host disease (aGvHD), the mechanisms regulating the proliferation and function of donor T cells remain unclear. Here, we show that activated donor T cells express galectin-3 (Gal-3) after allo-HCT. In both major and minor histocompatibility–mismatched models of murine aGvHD, expression of Gal-3 is associated with decreased T cell activation and suppression of the secretion of effector cytokines including IFN-γ and GM-CSF. Mechanistically, Gal-3 results in activation of NFAT signaling which can induce T cell exhaustion. Gal-3 overexpression in human T cells prevents severe disease by suppressing cytotoxic T cells in xenogeneic aGvHD models. Together these data identify the Gal-3-dependent regulatory pathway in donor T cells as a critical component of inflammation in aGvHD.

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