E-GEOD-34437
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-34437 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-34437-analysis-methods.tsv | Tabular | |||
| E-GEOD-34437-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-34437-configuration.xml | Xml | |||
| E-GEOD-34437-percentile-ranks.tsv | Tabular | |||
| E-GEOD-34437.condensed-sdrf.tsv | Tabular |
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Project description:Expression data from human renal allograft biopsies to investigate renal transplant rejection and failure
2025-01-24 | E-GEOD-21374 | ExpressionAtlas
Project description:Expression of the IL-17/Th17 axis in the development of acute renal allograft rejection
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Project description:Genesets for the IL-17 pathway and Th17 T-helper cell subtype showed increasing enrichment in 33 pre-transplant donor biopsies and 33 matching post-transplant biopsies from patients with increasing Banff grades of acute rejection (no signficant abnormalities, n=17; borderline, n=4; ARIA, n=7; ARIB, n=6) in gene set analysis using SAM (GSA, FDR 0.5; 1000 permutations, log rank regression) for a total of 3307 publically available and manually curated gene-sets. 14 genes of the IL-17 pathway gene-set and 132 genes of the Th17 gene set segregated patients according to their histological diagnosis by unsupervised hierarchical clustering and principal component analysis. This study demonstrates a significant role for the IL-17 pathway in the development of acute renal allograft rejection. Therapeutically targeting the IL-17 pathway presents a promising option in transplantation medicine and can be acchieved through drug reposittioning. Keywords: IL-17 pathway, drug repositioning, gene set enrichment analysis A total of 66 human renal allograft protocol biopsies were included in this study, 33 biopsies obtained at implantation prior to revascularization and 33 protocol biopsies obtained after transplantation. Whole genome expression profiles were assessed using microarrays. This dataset is part of the TransQST collection.
2014-01-01 | E-GEOD-34437 | biostudies-arrayexpress
Project description:A peripheral blood diagnostic test for acute rejection in renal transplantation.
2025-01-24 | E-GEOD-14346 | ExpressionAtlas
Project description:Transcriptomic analyses of renal allograft biopsies reveal conserved rejection signatures and molecular pathways
2025-01-24 | E-GEOD-9493 | ExpressionAtlas
Project description:Genesets for the IL-17 pathway and Th17 T-helper cell subtype showed increasing enrichment in 33 pre-transplant donor biopsies and 33 matching post-transplant biopsies from patients with increasing Banff grades of acute rejection (no signficant abnormalities, n=17; borderline, n=4; ARIA, n=7; ARIB, n=6) in gene set analysis using SAM (GSA, FDR 0.5; 1000 permutations, log rank regression) for a total of 3307 publically available and manually curated gene-sets. 14 genes of the IL-17 pathway gene-set and 132 genes of the Th17 gene set segregated patients according to their histological diagnosis by unsupervised hierarchical clustering and principal component analysis. This study demonstrates a significant role for the IL-17 pathway in the development of acute renal allograft rejection. Therapeutically targeting the IL-17 pathway presents a promising option in transplantation medicine and can be acchieved through drug reposittioning. Keywords: IL-17 pathway, drug repositioning, gene set enrichment analysis
2014-01-01 | GSE34437 | GEO
Project description:The study comprises various components: Samples TD: We aims to screen out different gene expression profile in donor biopsies after revascularization , We aims to predict renal allograft dysfunction early after transplantation. Samples AR, ATN, Tx: We aim to screen out different gene expression profile in acute rejection on the kidney. We aim to screen out different gene expression profile in acute tubular necrosis on the kidney. Results from the various study components can help to diagnose renal allograft dysfunction with different causes by distinct gene expression profile. Keywords: acute rejection, acute tubular necrosis, donor biopsies, renal allograft dysfunction Samples AR1-AR17: This study has been accomplished with 17 patients of acute rejection on the kidney.Technical replicates: 2 replicates Samples ATN1-ATN5: This study has been accomplished with 5 patients of acute tubular necrosis on the kidney. Technical replicates: 2 replicates Samples Tx1-Tx14: This study has been accomplished with 14 patients of stable renal function on the kidney.Tecnical replicates:2 replicates(except Tx12) Samples TD1-TD12: This study has been accomplished with 12 patients of donor tissue with stable function early after transplantation on the kidney.Technical replicates: 2 replicates Samples TD13-TD21: This study has been accomplished with 9 patients of donor tissue with renal dysfunction early after transplantation on the kidney.Technical replicates: 2 replicates
2011-02-02 | E-GEOD-26578 | biostudies-arrayexpress
Project description:CONTEXT Slowly progressive chronic tubulo-interstitial damage jeopardizes long-term renal allograft survival. Both immune and non-immune mechanisms are thought to contribute, but the most promising targets for timely intervention have not been identified. OBJECTIVE In the current study we seek to determine the driving force behind progressive histological damage of renal allografts, without the interference of donor pathology, delayed graft function and acute graft rejection. DESIGN We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. PATIENTS Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection. RESULTS In this highly cross-validated study, we demonstrate the significant association of established, ongoing and future chronic histological damage with regulation of adaptive immune gene expression (T-cell and B-cell transcript sets) and innate immune response gene expression (dendritic cell, NK-cell, mast cell and granulocyte transcripts). We demonstrate the ability of gene expression analysis to perform as a quantitative marker for ongoing inflammation with a wide dynamic range: from subtle subhistological inflammation prior to development of chronic damage, over moderate subclinical inflammation associated with chronic histological damage, to marked inflammation of Banff-grade acute T-cell mediated rejection. CONCLUSION Progressive chronic histological damage after kidney transplantation is associated with significant regulation of both innate and adaptive immune responses, months before the histological lesions appear. This study therefore corroborates the hypothesis that quantitative inflammation below the diagnostic threshold of classic T-cell or antibody-mediated rejection is associated with early subclinical stages of progressive renal allograft damage. We used microarrays to examine whole genome expression profiles in renal allograft protocol biopsies, and analyzed the correlation between gene expression and the histological appearance over time. The gene expression profiles in these protocol biopsies were then compared with gene expression of biopsies with acute T-cell mediated rejection. Human renal allograft biopsies (N=120) were included: 96 rejection-free protocol biopsies and 24 biopsies with T-cell mediated acute rejection.
2011-12-10 | E-GEOD-25902 | biostudies-arrayexpress
Project description:Compromised renal function after renal allograft transplantation often results in anemia in the recipient. Molecular mechanisms leading to anemia during acute rejection are not fully understood; inadequate erythropoietin production and iron deficiency have been reported to be the main contributors. To increase our understanding of the molecular events underlying anemia in acute rejection, we analyzed the gene expression profiles of peripheral blood lymphocytes (PBL) from four pediatric renal allograft recipients with acute rejection and concurrent anemia, using DNA microarrays containing 9000 human cDNA clones (representing 7469 unique genes). In these anemic rejecting patients, an 'erythropoiesis cluster' of 11 down-regulated genes was identified, involved in hemoglobin transcription and synthesis, iron and folate binding and transport. Additionally, some alloimmune response genes were simultaneously down-regulated. An independent data set of 36 PBL samples, some with acute rejection and some with concurrence of acute rejection and anemia, were analyzed to support a possible association between acute rejection and anemia. In conclusion, analysis using DNA microarrays has identified a cluster of genes related to hemoglobin synthesis and/or erythropoeisis that was altered in kidneys with renal allograft rejection compared with normal kidneys. The possible relationship between alterations in the expression of this cluster, reduced renal function, the alloimmune process itself, and other influences on the renal transplant awaits further analysis.
2005-11-01 | E-SMDB-2730 | biostudies-arrayexpress
Project description:Renal dendritic cells play key roles in renal homeostasis and during kidney allograft rejection. Microarray analysis aims to evaluate whether dendritic cells modulate their gene expression profile in relation to their distribution in the different renal compartments (with varying biophysical characteristics), under homeostatic conditions and during acute renal allograft rejection (3 days post-transplantation).
2015-02-04 | GSE65564 | GEO