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Single cell transcriptome mapping identifies a local innate B cell population driving chronic rejection after lung transplantation

ABSTRACT: Single cell transcriptome mapping identifies a local innate B cell population driving chronic rejection after lung transplantation

PROVIDER: PRJNA700655 | ENA |

REPOSITORIES: ENA

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Single cell transcriptome mapping identifies a local innate B cell population driving chronic rejection after lung transplantation

Project description:Bronchiolitis obliterans syndrome (BOS) is the main reason for poor outcomes after lung transplantation (LTx). We and others have recently identified B cells as major contributors to BOS after LTx. The extent of B cell heterogeneity and the relative contributions of B cell subpopulations to BOS, however, remain entirely unclear. Here, we provide a comprehensive analysis of cell population changes and their gene expression patterns during chronic rejection after orthotopic LTx in mice. Out of a total of 11 major cell types, Mzb1-expressing plasma cells (PCs) were the most prominently increased population in BOS lungs. These findings were validated in two different cohorts of human BOS after LTx. A Bhlhe41, Cxcr3, Itgb1-triple positive-B cell subset, also expressing classical markers of the innate-like B-1 B cell population, served as the progenitor pool for Mzb1+ PCs. This subset accounted for the increase in IgG2c production within BOS lung grafts. A genetic lack of immunoglobulins decreased BOS severity after LTx. In summary, we provide a detailed analysis of cell population changes during BOS. IgG-positive PCs and their progenitors – an innate B cell subpopulation – are the major source of local antibody production and a significant contributor to BOS after LTx.

2022-07-25 | GSE166386 | GEO

Single-cell transcriptome mapping identifies a local, innate B cell population driving chronic rejection after lung transplantation.

Project description:Bronchiolitis obliterans syndrome (BOS) is the main reason for poor outcomes after lung transplantation (LTx). We and others have recently identified B cells as major contributors to BOS after LTx. The extent of B cell heterogeneity and the relative contributions of B cell subpopulations to BOS, however, remain unclear. Here, we provide a comprehensive analysis of cell population changes and their gene expression patterns during chronic rejection after orthotopic LTx in mice. Of 11 major cell types, Mzb1-expressing plasma cells (PCs) were the most prominently increased population in BOS lungs. These findings were validated in 2 different cohorts of human BOS after LTx. A Bhlhe41, Cxcr3, and Itgb1 triple-positive B cell subset, also expressing classical markers of the innate-like B-1 B cell population, served as the progenitor pool for Mzb1+ PCs. This subset accounted for the increase in IgG2c production within BOS lung grafts. A genetic lack of Igs decreased BOS severity after LTx. In summary, we provide a detailed analysis of cell population changes during BOS. IgG+ PCs and their progenitors - an innate B cell subpopulation - are the major source of local Ab production and a significant contributor to BOS after LTx.

| S-EPMC9675462 | biostudies-literature

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.

2022-06-30 | GSE206801 | GEO

Molecular Characterization of Acute Cellular Rejection Occurring during Intentional Immunosuppression Withdrawal in Liver Transplantation

Project description:Acute cellular rejection occurs frequently during the first few weeks following liver transplantation. During this period its molecular phenotype is confounded by pro-inflammatory events elicited by surgery, ischemia-reperfusion injury and early post-transplant complications. To unambiguously define the molecular profile associated with rejection we collected sequential biological specimens from liver transplant patients at least 3 years after transplantation who developed rejection while enrolled in trials of intentional immunosuppression withdrawal Transcriptomic RISET 2.0 chips were employed using portal blood vein from 37 liver trasplant patients.Two timepoints were selected: before immunosupressive weaning and rejection time point.

2016-06-01 | E-GEOD-70305 | biostudies-arrayexpress

Donor Macrophages Modulate Rejection after Heart Transplantation

Project description:Donor Macrophages Modulate Rejection after Heart Transplantation

| PRJNA852221 | ENA

Molecular Characterization of Acute Cellular Rejection Occurring during Intentional Immunosuppression Withdrawal in Liver Transplantation

2016-06-01 | GSE70305 | GEO

A single cell analysis of allograft rejection and tolerance using mouse solid organ transplantation models

Project description:Solid organ transplantation in the mouse is a powerful research tool that has provided a pathway to find important mechanistic insights into the regulation of allograft injury, allograft immunopathology, and transplant rejection/tolerance, and that has unique advantages over transplantation in larger species, due to the well characterization of mouse genome and availability of genetically modified animals. However, setup of mouse liver, heart and kidney transplantation is a technically demanding surgical procedure, especially the orthotopic liver transplantation in mouse. Here, we performed Microwell-based single cell RNA-seq of three mouse organ transplantation models (liver, heart and kidney). Comparison of lymphocytes, parenchyma cells and peripheral blood mononuclear cells in liver, heart and kidney revealed distinct immune microenvironment at acute rejection and tolerance state respectively. Single-cell transcriptome analysis of mouse allograft without immunosuppressive drugs provided rich resources to help understand functioning solid-organ transplantation in human.

2022-11-18 | GSE189069 | GEO

Dysregulated regulatory T cell responses expand fibroblasts and lead to chronic rejection after heart transplantation

Project description:Chronic rejection after organ transplantation manifests as immunosuppressant-resistant graft vascular remodeling and fibrosis, which remains the dominant driver of mortality after the first year of heart transplantation. Single-cell RNAseq analysis of MHCII-mismatched heart transplants developing chronic rejection identified graft IL-33 as a stimulator of tissue repair pathways in infiltrating myeloid cells and regulatory T cells (Tregs). Using IL-33-deficient donor mice, it was revealed that graft fibroblast-derived IL-33 potently induced Amphiregulin (Areg) expression by recipient Treg. Areg is an epidermal growth factor secreted by multiple immune cells to shape immunomodulation and tissue repair. In particular, Areg is proposed to play a major role in Treg-mediated muscle, epithelium, and nerve repair. Assessing recipient mice with Treg-specific deletion of Areg demonstrated that this pathway surprisingly contributes to chronic rejection. Specifically, heart transplants from recipients with Areg-deficient Tregs exhibited less vasculopathy and vessel-associated fibrotic niches infiltrated by recipient T cells. Mechanistically, we show that Areg does not impact Treg suppressive function, but that IL-33 mediated Treg-secretion of Areg increases fibroblast proliferation and migration. In total, these studies identify how a dysregulated repair response involving interactions between IL-33+ fibroblasts in the allograft and recipient Treg contributes to the progression of chronic rejection.

2024-12-02 | GSE235871 | GEO

Microarray screening for microRNAs differentially expressed in whole blood samples of patients with clinically significant rejection after liver transplantation

Project description:To investigate whether differentially expressed microRNAs in peripheral blood could be associated with clinically significant, histologically proven acute cellular rejection after liver transplantation, a microRNA microarray screening was performed with RNA isolated from PaxGene whole blood samples from patients with ACR within the first three postoperative weeks and from patients without clinical signs of rejection within the first 6 months after transplantation.

2016-12-24 | GSE65492 | GEO

ALLoreactive T-Cell receptOr RePertoire in kidnEy tranSplantation

Project description:A prospective study for investigating the T-cell receptor (TCR) repertoire in T-cell mediated rejection (TCMR) after kidney transplantation. The pre-formed donor-reactive TCR repertoire was tracked in blood and tissue of patients after kidney transplantation and characteristics of TCR repertoires from patients experiencing a rejection were compared to patients with no histopathological signs of rejection.

| EGAS00001005299 | EGA

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