Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1209112 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31961500.fastq.gz | Fastqsanger.gz | |||
| SRR31961500_1.fastq.gz | Fastqsanger.gz | |||
| SRR31961500_2.fastq.gz | Fastqsanger.gz | |||
| SRR31961501.fastq.gz | Fastqsanger.gz | |||
| SRR31961501_1.fastq.gz | Fastqsanger.gz |
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Project description:Reconstitution of stem cells and enhancement of the barrier function of the gastrointestinal (GI) tract is critical to the resolution of intestinal acute graft-versus-host disease (aGvHD). Previously, our group has shown in murine models that type II innate lymphoid cells (ILC2) cells generate proteins in the GI tract that enhanced GI tract barrier function and diminished the expansion and function of pro-inflammatory donor cells when given to allogeneic stem cell transplant recipients. Therefore, the infusion of donor ILC2 cells could treat or prevent GI tract acute GvHD, but for this approach to be clinically applicable, robust expansion of a homogenous population of human ILC2 cells is needed. Here, we describe a method for the rapid expansion of a uniform population of human ILC2 cells which decrease GvHD in (NOD scid gamma mouse) NSG mice. The addition of IL-4 to the culture was critical to prevent the expansion of pro-inflammatory ILC1-like cells. Our approach should allow for the evaluation of human ILC2 cells to treat therapy-resistant GI tract acute GvHD.
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Project description:CD4+Foxp3+ regulatory T cells (Treg) are a subpopulation of T cells, which regulate the immune system and enhance immune tolerance after transplantation. Donor-derived Treg prevent the development of lethal acute graft and host disease (GVHD) in murine models of allogeneic hematopoietic cell transplantation. It was reported that a single treatment of the agonistic antibody to Death receptor 3 (DR3) in donor mice resulted in the expansion of donor derived Treg and prevented acute GVHD, although the precise role of DR3 signaling in GVHD has not been elucidated. We analyzed the gene expression profile, immune phenotype, and function of DR3-activated Treg in a murine model of allogeneic hematopoietic cell transplantation. CD4+Foxp3+ Treg were sorted from the mice stimulated with anti-DR3 or control antibody using fluorescence-activated cell sorter for RNA extraction and hybridization on Affymetrix microarrays.
2016-06-28 | E-GEOD-83743 | biostudies-arrayexpress
Project description:The aim of this study is to assess the Fecal Microbiota Transplantation (FMT) efficacy in the prevention of allogeneic hematopoietic stem cell transplantation (allo-HSCT) complications and particularly Graft versus Host Disease (GvHD).
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Project description:Reconstitution of stem cells and enhancement of the barrier function of the gastrointestinal (GI) tract is critical to the resolution of intestinal acute graft-versus-host disease (aGvHD). Previously, our group has shown in murine models that type II innate lymphoid cells (ILC2) cells generate proteins in the GI tract that enhanced GI tract barrier function and diminished the expansion and function of pro-inflammatory donor cells when given to allogeneic stem cell transplant recipients. Therefore, the infusion of donor ILC2 cells could treat or prevent GI tract acute GvHD, but for this approach to be clinically applicable, robust expansion of a homogenous population of human ILC2 cells is needed. Here, we describe a method for the rapid expansion of a uniform population of human ILC2 cells which decrease GvHD in (NOD scid gamma mouse) NSG mice. The addition of IL-4 to the culture was critical to prevent the expansion of pro-inflammatory ILC1-like cells. Our approach should allow for the evaluation of human ILC2 cells to treat therapy-resistant GI tract acute GvHD.
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Project description:CD4+Foxp3+ regulatory T cells (Treg) are a subpopulation of T cells, which regulate the immune system and enhance immune tolerance after transplantation. Donor-derived Treg prevent the development of lethal acute graft and host disease (GVHD) in murine models of allogeneic hematopoietic cell transplantation. It was reported that a single treatment of the agonistic antibody to Death receptor 3 (DR3) in donor mice resulted in the expansion of donor derived Treg and prevented acute GVHD, although the precise role of DR3 signaling in GVHD has not been elucidated. We analyzed the gene expression profile, immune phenotype, and function of DR3-activated Treg in a murine model of allogeneic hematopoietic cell transplantation.
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Project description:Inducible co-stimulator (ICOS) interaction with its ligand (ICOSL) is involved in several T cell effector functions. While blockade of ICOS:ICOSL interaction in chronic graft versus host disease (GVHD) seems benefi cial, results for acute GVHD remain controversial. To further elucidate its role in acute GVHD, C57BL / 6 mice were lethally irradiated and reconstituted with allogeneic spleen cells in the absence or presence of ICOSL-blocking mAb. Mice reconstituted with allogeneic spleen cells experienced severe GVHD and died untreated within 6 – 9 days after transplantation. Mice treated with an anti-ICOSL mAb starting from day 3 after transplantation gained weight again and survived for at least additional 12 days, although the treatment was already stopped at day 11 after transplantation. In contrast, the anti-ICOSL treatment starting from day 0 did not prevent GVHD. The diff erence between therapeutic (day 3) and prophylactic (day 0) anti-ICOSL treatment was independent of CD25 + CD4 + regulatory T cells since their depletion did not abrogate the therapeutic eff ect of ICOSL blockade. Microarray analysis revealed IFN- γ and chemokine up-regulation in spleen cells of prophylactically treated mice, emphasizing kinetic dependence of acute GVHD modulation via blockade of ICOS:ICOSL interaction.
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Project description:In comparison with allogeneic hematopoietic stem cell transplantation using other sources, umbilical cord blood transplantation (UCBT) offers substantial clinical advantages including a lower incidence and severity of acute graft-versus-host disease (GVHD) despite the use of allogeneic UCB stem cells with more disparate HLA. However, detailed pathophysiology of acute GVHD developed after UCBT has not yet been clarified. Here, we examined the roles of inflammatory cells in the pathogenesis of acute GVHD following UCBT, by expression profiling of a total of 615 genes in each of 4 subsets (CD4+, CD8+, CD14+, and CD56+) of peripheral blood mononuclear cells (PBMCs), which were taken from 5 patients with hematologic malignancy, in whom acute GVHD had developed after UCBT. By comparing expression profiles measured during acute GVHD with those measured upon discharge (recovery phase), for each subset of PBMCs, we identified immuno-regulatory genes which were assumed to be linked to the pathogenesis of acute GVHD. Keywords: disease state analysis CD4+, CD8+, CD14+, and CD56+ cell subsets were isolated from the peripheral blood mononuclear cells (PBMCs) of 5 patients with hematologic malignancy, in whom acute GVHD had developed after cord blood transplantation. PBMCs were taken twice â during acute GVHD phase and upon discharge (recovery phase), from each patient. By using a custom-made fibrous oligonucleotide DNA microarray Genopal (Mitsubishi Rayon), we compared expression profiles of 615 unique genes measured during acute GVHD with those measured upon discharge (recovery phase), for each subset of PBMCs.
2010-05-15 | E-GEOD-10513 | biostudies-arrayexpress
Project description:In comparison with allogeneic hematopoietic stem cell transplantation using other sources, umbilical cord blood transplantation (UCBT) offers substantial clinical advantages including a lower incidence and severity of acute graft-versus-host disease (GVHD) despite the use of allogeneic UCB stem cells with more disparate HLA. However, detailed pathophysiology of acute GVHD developed after UCBT has not yet been clarified. Here, we examined the roles of inflammatory cells in the pathogenesis of acute GVHD following UCBT, by expression profiling of a total of 595 genes in each of 4 subsets (CD4+, CD8+, CD14+, and CD56+) of peripheral blood mononuclear cells (PBMCs), which were taken from 3 patients with hematologic malignancy, in whom acute GVHD had developed after UCBT. We compared expression profiles measured during acute GVHD with those measured opon discharge (recovery phase), for each subset of PBMCs to identify immuno-regulatory genes which were assumed to be linked to the pathogenesis of acute GVHD. Keywords: disease state analysis Peripheral blood mononuclear cells (PBMCs) were taken from 3 patients with hematologic malignancy, in whom acute GVHD had developed after cord blood transplantation. CD4+, CD8+, CD14+, and CD56+ cell subsets were isolated from the PBMCs of 2 patients, while only CD8+ and CD56+ cell subsets were isolated from the PBMCs of a patient. PBMCs were taken twice - during acute GVHD phase and upon discharge (recovery phase), from each patient. By using a custom-made fibrous oligonucleotide DNA microarray Genopal (Mitsubishi Rayon), we compared expression profiles of 595 unique genes measured during acute GVHD with those measured upon discharge (recovery phase), for each subset of PBMCs.
2010-05-15 | E-GEOD-10512 | biostudies-arrayexpress
Project description:Graft-versus-host disease (GvHD) is still one of the major complications following allogeneic stem cell transplantation (SCT) triggered by alloreactive donor T cells. Whereas murine data have clearly shown the beneficial effects of regulatory T cells (Tregs) on the development of GvHD, data from the human system are rare mainly due to low cell numbers of circulating or organ-infiltrating Tregs in lymphopenic patients. Here, we present a comparative analysis of Tregs from patients with and without acute/ chronic GvHD designed as a dynamical approach studying the whole genome profile over the first 6 months after SCT. For this purpose, blood samples were collected monthly for FACS-based isolation of CD4+CD25highCD127low/- Tregs. The Treg transcriptome showed a high stability in the first half year representing the most sensitive time window for tolerance induction. However, the comparison of the Treg transcriptome from patients with and without GvHD uncovered regulated gene transcripts that point to a reduced suppressive function of Tregs with diminished migration capacity to the target organs likely contributing to the development of GvHD. These findings highlight the critical role of human Tregs in the pathophysiology of GvHD and identify novel targets for the manipulation of Tregs to optimize cellular immune intervention strategies. Keywords: cell type comparison Relative gene expressions were determined by normalized intensity values. GeneSpring analysis was performed using the Treg transcriptome data with following comparisons: no GvHD d90 versus no GvHD d150, no GvHD d90 versus acute GvHD, no GvHD d150 versus chronic GvHD, acute GvHD versus chronic GvHD, acute GvHD versus GvHD d90 and chronic GvHD versus GvHD d150 (Figure 2). Cut-off was a transcript fold change of 2 or -2 in at least one comparison. Student´s t-test was used to identify significant expression changes.
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