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Functional Transition of CD11b+CD33+HLA-DR-/lowCD14- G-MDSC: Immunostimulation to Immunosuppression Post Allo-HSCT

ABSTRACT: Functional Transition of CD11b+CD33+HLA-DR-/lowCD14- G-MDSC: Immunostimulation to Immunosuppression Post Allo-HSCT

PROVIDER: PRJNA1081857 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28151100_1.fastq.gz	Fastqsanger.gz
	SRR28151100_2.fastq.gz	Fastqsanger.gz
	SRR28151101_1.fastq.gz	Fastqsanger.gz
	SRR28151101_2.fastq.gz	Fastqsanger.gz
	SRR28151102_1.fastq.gz	Fastqsanger.gz

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Functional Transition of CD11b+CD33+HLA-DR-/lowCD14- G-MDSC: Immunostimulation to Immunosuppression Post Allo-HSCT

Project description:The prediction of acute graft-versus-host disease (aGvHD) post allogeneic hematopoietic stem cell transplantation (allo-HSCT) is critical for treatment decisions. The granulocytic myeloid-derived suppressor cells (G-MDSCs) show a fast recovery post-transplantation and constituted the major part of peripheral blood in the early phase after allo-HSCT. These cells were previously believed to exhibit immunosuppressive properties. However, they also promote inflammation under specific conditions. Thus, we conducted a comprehensive study of G-MDSCs from 82 patients after allo-HSCT within 90 days to elucidate the role of them in post-transplantation immunity. Strikingly, our results showed that G-MDSCs promoted inflammation in the early-stage, by facilitating cytokine secretion and proliferation of T cells, as well as their differentiation into pro-inflammatory T helper subsets. At day 28, patients with a higher number of G-MDSCs exhibited an increased risk of developing aGvHD. Besides, adoptive transfer of G-MDSCs from patients into humanized mice exacerbated aGvHD. However, at day 90, G-MDSCs showed immunosuppressive features, characterized by upregulated expression of indoleamine 2,3-dioxygenase gene and interleukin-10 secretion, coupled with the inhibition of T cell proliferation. Furthermore, transcriptional analysis of G-MDSCs at day 28 and day 90 revealed that a total of 1445 genes were differentially expressed. Genes linked to the endoplasmic reticulum stress were upregulated in patients without aGvHD. After the genetic overlap analysis, DERL1 may be the hub-gene. Our findings elucidate the alteration in the immune characteristics of G-MDSCs within the first 90 days post allo-HSCT. Moreover, the quantity of G-MDSCs at day 28 could serve as a predictive indicator for aGvHD.

2024-06-25 | GSE260477 | GEO

CLL relapse after allo-HSCT

Project description:CLL relapse after allo-HSCT

| PRJNA615002 | ENA

CLL relapse after allo-HSCT

Project description:CLL relapse after allo-HSCT

| PRJNA615003 | ENA

Gene expression analysis of CD11c+ splenic DCs day 7 after allo-HSCT.

Project description:The goal of our study is to determine whether Atg16L1 deficiency leads to differences in the transcriptional profile of CD11c+ Dendritic Cells, ultimately leading to an increased inflammatory phenotype. CD11c+ cell sorted splenic DCs were isolated from 8 week old WT and Atg16L1 hypomorphic mice from spleens of allo-HSCT recipients on day 7 were placed directly into TRIzol LS (Invitrogen). mRNA was isolated, amplified, and hybridized to an Affymetrix GeneChip (MOE430A).

2014-09-19 | E-GEOD-61560 | biostudies-arrayexpress

A clinical trial of Vedolizumab vs. placebo (dummy drug) for the prevention of intestinal Acute Graft Versus Host Disease (aGvHD), in patients undergoing allo-HSCT for a hematologic malignancy, (cancers that affect the blood and/or lymphatic system).

Project description:Main Objective: To evaluate the efficacy of vedolizumab when added to background aGvHD prophylaxis regimen compared to placebo and background aGvHD prophylaxis regimen on intestinal aGvHD-free survival by Day +180 in subjects who receive allo-HSCT as treatment for a hematologic malignancy or myeloproliferative disorder. Primary end point(s): The primary endpoint is intestinal aGvHD-free survival by Day +180 after allo HSCT. Intestinal aGvHD is defined as Stage 1-4 intestinal involvement per Acute Graft versus-Host Disease Clinical Stage criteria.

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Project description:Myeloid-derived suppressor cells (MDSC) is a heterogeneous population of cells that can negatively regulate T-cell function. As opposed to murine MDSC, which are characterized as Gr-1+CD11b+ cells, human MDSC are not so clearly defined due to lack of specific markers. Our lab has previously identified a new subset of MDSC as CD14+HLA-DR-neg/low cells from PBMC. CD14+HLA-DR-neg/low MDSC not only suppress proliferation and IFN-gamma secretion of autologous T cells, but also induce CD25+Foxp3+ regulatory T cells that are suppressive in vitro, whereas the counterpart CD14+HLA-DR-high monocytes don’t have the effect. In this study, we compare the immune-related gene expression between CD14+HLA-DR-neg/low MDSC and CD14+HLA-DR-high monocytes to better characterize the difference between these two populations and to find new potential specific marker for human MDSC. PBMC were isolated from fresh blood healthy donor by density centrifugation. CD14+ cells were isolated by AutoMACS CD14 microbeads using a AutoMACS (Miltenyi), and then stained with CD14 and HLA-DR antibodies. MDSC and monocytes control cells were sorted as CD14+ HLA-DR-neg/low and CD14+HLA-DR-high cells respectively. The sorted two populations were immediately frozen in liquid nitrogen and shipped to the company on dry ice for RNA isolation and further microarray.

2011-09-08 | E-GEOD-32001 | biostudies-arrayexpress

Targeting Interleukin-2-Inducible T-cell Kinase (ITK) differentiates GVL and GVHD in allo-HSCT

Project description:Allogeneic hematopoietic stem cell transplantation is a potentially curative procedure for many malignant diseases. Donor T cells prevent disease recurrence via graft-versus-leukemia (GVL) effect. Donor T cells also contribute to graft-versus-host disease (GVHD), a debilitating and potentially fatal complication. Novel treatment strategies are needed which allow preservation of GVL effects without causing GVHD. Using murine models, we show that targeting IL-2-inducible T cell kinase (ITK) in donor T cells reduces GVHD while preserving GVL effects. Both CD8+ and CD4+ donor T cells from Itk-/- mice produce less inflammatory cytokines and show decrease migration to GVHD target organs such as the liver and small intestine, while maintaining GVL efficacy against primary B-cell acute lymphoblastic leukemia (B-ALL). Itk-/- T cells exhibit reduced expression of IRF4 and decreased JAK/STAT signaling activity, but upregulating expression of Eomesodermin (Eomes) and preserve cytotoxicity, necessary for GVL effect. Transcriptome analysis indicates that ITK signaling controls chemokine receptor expression during alloactivation, which in turn affects the ability of donor T cells to migrate to GVHD target organs. Our data suggest that inhibiting ITK could be a therapeutic strategy to reduce GVHD while preserving the beneficial GVL effects following allo-HSCT treatment.

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2011-09-09 | GSE32001 | GEO

Targeting Interleukin-2-Inducible T-cell Kinase (ITK) differentiates GVL and GVHD in allo-HSCT

Project description:Targeting Interleukin-2-Inducible T-cell Kinase (ITK) differentiates GVL and GVHD in allo-HSCT

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Metagenomics of Autologous Fecal Microbiota Transplantation in allo-HSCT Patients at MSKCC

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