Genome-wide analysis of gene expression variation in CD4+ T cells from patients with active rheumatoid arthritis (RA).
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE55468 | GEO | 2014/05/26
SECONDARY ACCESSION(S): PRJNA239799
REPOSITORIES: GEO
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Project description:Analysis of the regulatory architecture of gene expression variation in CD4+ T cells from patients with active RA. We have integrated gene expression with genotyping data in order to identify eQTLs that characterize the gene expression of CD4+ T cells in active RA. CD4+ T cell RNA was extracted from 26 patients with active RA. All samples were used to study the genetic regulatory mechanisms of CD4+ T cells in active Rheumatoid Arthritis.
2014-05-26 | E-GEOD-55468 | biostudies-arrayexpress
Project description:Rheumatoid arthritis (RA) is a systemic autoimmune disease and its underlying molecular mechanisms are still poorly understood. Previously a CD4 T-cell microarray study has only focused arthritis patients. We aimed to compare the molecular profiles of active RA versus healthy control in CD4 T cells. We used microarrays to detail the global programme of gene expression in active RA and healthy control.
2017-02-13 | GSE56649 | GEO
Project description:To identify susceptibility genes concerning copy number variations (CNVs) in rheumatoid arthritis (RA), a case-control genome-wide CNV analyses was carried out by Roche Nimblegen array-based CGH. In this study, 15 RA patients and 1 control (Non-RA) were included.
2010-06-09 | GSE22108 | GEO
Project description:Accelerating Medicines Partnership-Rheumatoid Arthritis (AMP-RA)
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Project description:Genotyping was performed using a custom-designed Illumina 384-SNP VeraCode microarray (Illumina) to determine possible associations of genes encoding PADI1, PADI2, PADI3, PADI4, PADI6, PRKD3, Gc, GLRX,CDSN, PSORS1C1, TXNDC5, CA1, bub3, SORBS1, VDR,SERPNA1, PCSK6, DNAH9 to rheumatoid arthrities (RA) and ankylosing spondylitis (AS). We previously found that encoding genes of PADI1, PADI2, PADI3, PADI4, PADI6, PRKD3, Gc, GLRX,CDSN, PSORS1C1, TXNDC5, CA1, bub3, SORBS1, VDR, SERPNA1, PCSK6 and DNAH9 could be associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). We used illumina customer designed microarray to verify the above finding with an increased numbers of samples. Genotyping was performed using a custom-designed Illumina 384-SNP VeraCode microarray (Illumina) to determine possible associations of genes encoding PADI1, PADI2, PADI3, PADI4, PADI6, PRKD3, Gc, GLRX,CDSN, PSORS1C1, TXNDC5, CA1, bub3, SORBS1, VDR, SERPNA1, PCSK6, DNAH9 to RA and AS. A case-control study was performed with 51 AS patients, 266 rheumatoid arthritis (RA) and 163 health controls. Tag single nucleotide polymorphisms (tag SNPs) across the above genes were determined by searching the HapMap database. The tag SNPs were selected on the basis of linkage disequilibrium patterns observed in the Han Chinese in Beijing (CHB) samples that were genotyped as a part of the International HapMap Project. Only SNPs with a minor allele frequency of greater than 5% with a pair-wise r2 ≥ 0.8 in the HapMap were considered. SNPs that were in exons and untranslated regions (UTR), as well as promoters and introns within 500 bp of exons were also selected. Candidate SNPs were submitted to Illumina for a design score. The Illumina Assay Design Tool filtered out SNPs that were not suitable for the Illumina platform. Finally, 382 SNPs with a design score of “1” were selected. 382 SNPs within PADI1, PADI2, PADI3, PADI4, PADI6, PRKD3, Gc, GLRX,CDSN, PSORS1C1, TXNDC5, CA1, bub3, SORBS1, VDR,SERPNA1, PCSK6, DNAH9 encoding genes were selected. Genotyping was performed using Illumina VeraCode microarray in a case-control study including 51 AS patients, 266 rheumatoid arthritis (RA) and 163 health controls We performed genotyping using a custom-designed Illumina 384-SNP VeraCode microarray (Illumina). Peripheral blood samples were collected from patients with RA (n=266, 183 female) and AS (n=51, 10 female). RA patients had a mean age of 51.7 years, while AS patients had a mean age of 35.9 years. A total of 163 (60 female) healthy individuals with a mean age of 48.0 years were blood donors. Blood samples were put into Monovette tubes containing 3.8% sodium citrate. The genotyping was conducted with the BeadXpress Reader using the Illumina VeraCode GoldenGate Assay kit. 500 ng of sample DNA were used per assay. Genotype clustering and calling were performed using BeadStudio software (Genomestudio V2010.2 Genotyping module V1.6) (Illumina). This work was completed at the Beijing Institute of Genomics.
2012-07-22 | E-GEOD-39428 | biostudies-arrayexpress
Project description:We study a new pathogenic, glycolytic PD1+ B cell population in sites of inflammation of patients with Rheumatoid Arthritis (RA).
2020-09-30 | GSE154988 | GEO
Project description:Objective: Conflicting evidence exists regarding the suppressive capacity of Tregs from the peripheral blood (PB) of patients with rheumatoid arthritis (RA). Our aim was to determine whether Tregs are intrinsically defective in RA using a wide range of read-out assays. Methods: CD3+CD4+CD25+CD127low Tregs from CD45RO+ and CD45RA+ compartments of PB from patients with RA and healthy controls (HC) were analysed for phenotype, cytokine expression profile (ex vivo and after in vitro stimulation), suppression of effector T-cell proliferation and cytokine production, suppression of monocyte-derived cytokine/chemokine production, and gene expression profiling. Results: No differences were observed between patients with RA and HC regarding Treg frequency, ex vivo phenotype (CD4, CD25, CD127, CD39, CD161) or pro-inflammatory cytokine profile (IL-17, IFN-gamma, TNF-alpha). FOXP3 expression was increased in Tregs from RA blood. The ability of Tregs to suppress T-cell proliferation or cytokine (IFN-gamma, TNF-alpha) production upon co-culture with autologous CD45RO+ effector T-cells and monocytes was not significantly different between patients with RA and HC. CD45RO+ Tregs from RA blood showed a slightly impaired ability to suppress production of some cytokines/chemokines by autologous LPS-activated monocytes (IL-1-beta, IL-1Ra, IL-7, CCL3, CCL4), but this was not true for all patients and other cytokines/chemokines (TNF-alpha, IL-6, IL-8, IL-12, IL-15, CCL5) were suppressed in the majority of patients similarly to HC. Finally, gene expression profiling of CD45RA+ or CD45RO+ Tregs from PB revealed no statistically significant differences between patients with RA and HC. Conclusions: Our findings suggest that Tregs isolated from PB of patients with RA are not intrinsically defective.
2015-09-05 | GSE65010 | GEO
Project description:Rheumatoid arthritis (RA) is a heterogeneous disease. We used cDNA microarray technology to subclassify RA patients and disclose disease pathways in rheumatoid synovium. Hierarchical clustering of gene expression data identified two main groups of tissues (RA-I and RA-II). A total of 121 genes were significantly higher expressed in the RA-I tissues, whereas 39 genes were overexpressed in the RA-II tissues. Among the 121 genes overexpressed in RA-I tissues, a relative majority of nine genes are located on chromosome 6p21.3. An interpretation of biological processes that take place revealed that the gene expression profile in RA-I tissues is indicative for an adaptive immune response. The RA-II group showed expression of genes suggestive for fibroblast dedifferentiation. Within the RA-I group, two subgroups could be distinguished; the RA-Ia group showed predominantly immune-related gene activity, while the RA-Ib group showed an additional higher activity of genes indicative for the classical pathway of complement activation. All tissues except the RA-Ia subgroup showed elevated expression of genes involved in tissue remodeling. These results confirm the heterogeneous nature of RA and suggest the existence of distinct pathogenic mechanisms that contribute to RA. The differences in expression profiles provide opportunities to stratify patients based on molecular criteria. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs
2005-12-15 | GSE3824 | GEO
Project description:MicroRNAs (miRNAs) have been implicated as fine-tuning regulators controlling diverse biological processes at the level of posttranscriptional repression. Dysregulation of miRNAs has been described in various disease states, including inflammatory autoimmune diseases. By using high-throughput microRNA profiling analysis, we identified a series of miRNAs dysregulated in local inflammatory lesions of human patients with autoimmune diseases such as RA. We isolated the synovial tissues from four RA patients as well as from two normal people (victims of accidental injury) and two osteoarthristis (OA) patients as controls for comparison. Total RNA was extracted for the TaqManM-BM-. Low Density Assay v3.0
2012-12-19 | E-GEOD-37425 | biostudies-arrayexpress
Project description:RA and RA-ILD metagenome
| PRJEB62405 | ENA