The Regulation of IFN Type I Pathway Related Genes RSAD2 and ETV7 Specifically Indicate Antibody-Mediated Rejection After Kidney Transplantation
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PROVIDER: PRJNA493832 | ENA |
REPOSITORIES: ENA
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Project description:We performed total RNA-Seq and compared expression levels of genes of whole blood cells isolated from patients after kidney transplantation with stable graft function, antibody mediated- and t cell mediated graft rejection.
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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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Project description:In this study, we examined transcriptional profiles from 3 different microarray platforms, across 103 peripheral blood samples with and without acute rejection, to find a critical gene-set for the diagnosis of acute renal rejection that matched biopsy diagnosis, irrespective of patient demographics, clinical confounders, concomitant infection, immunosuppression usage or sample processing methods. We hypothesized that changes in peripheral blood expression profiles correlate with biopsy-proven rejection, and that these changes could be used as biomarkers for the diagnosis and prediction of acute rejection. We performed cross-sectional microarray analysis of 103 matched peripheral blood samples collected at a single time point, timed with a biopsy where acute rejection was either confirmed as present (60 AR samples) or absent (62 STA samples). The samples were hybridized to one of 3 microarray platforms: Affymetrix (n=75 the 54K HG-U133_Plus2 Array), Agilent (n=26, 44K oligo Array) and cDNA array (n=21, ~30K cDNA). Of 103 samples, 14 were used on both Affy and Agilent arrays; 1 was used in cDNA and Agilent array and 2 were used across 3 array platforms. Microarray data generated from 3 array platforms were cross-compared, by mapping common and overlapping transcripts to Human Gene Organization (HUGO) gene names. Significant gene lists on each platform were identified using Significant Analysis of Microarray (SAM, ref) with a common significance threshold of a false discovery rate (FDR) of <10%.This set contains the data for samples hybridized to Affymetrix arrays. Disease State: Acute Rejection (AR#sampleid) or Stable (S#sampleid) samples. This dataset is part of the TransQST collection.
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Project description:Kidney transplant injury processes are associated with molecular changes in renal tissue, primarily related to immune cell activation and infiltration. How these processes are reflected by molecular alterations in circulating immune cells is poorly understood. We performed RNA-sequencing on 384 biobanked blood samples from four transplant centers, taken at time of a kidney allograft biopsy, selected for their phenotype (acute T cell- and antibody-mediated rejection, polyomavirus-associated nephropathy, and control). We performed differential expression analysis and pathway analysis per phenotype. In peripheral blood, differentially expressed genes in rejection vs. no rejection samples demonstrated upregulation of glucocorticoid receptor and NOD-like receptor signaling pathways. Pathways enriched in antibody-mediated rejection were strongly immune-specific, whereas pathways enriched in T cell-mediated rejection were less immune related. Differentially expressed genes in polyoma viremia and polyomavirus-associated nephropathy were similar and demonstrated upregulation of mitochondrial dysfunction and interferon signaling pathways. Our results highlight the immune activation pathways in peripheral blood leukocytes at time of antibody-mediated rejection and polyomavirus nephropathy and provide a framework for future therapeutic interventions.
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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
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