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RA-Map, A multi-omic survey of whole blood and subsets in early rheumatoid arthritis and vaccine study controls

ABSTRACT: Rheumatoid arthritis (RA) is a chronic inflammatory disorder of unknown aetiology characterised by synovial inflammation with variable disease severity and drug responsiveness. To investigate the molecular heterogeneity and pathogenesis of RA, we performed a comprehensive clinical and molecular profile of 267 RA patients for up to 18 months to establish a high quality biobank of barcoded samples that included plasma, serum, peripheral blood cells, whole blood RNA, RNA from lymphocyte and monocyte subsets, genomic DNA and urine. We have performed extensive multi-omic immune phenotyping, including genomic, metabolomic, proteomic, transcriptomic and auto-antibody profiling. We anticipate that these detailed clinical and molecular data will serve as a fundamental resource for the development and application of targeted therapies for RA and reveal further insights into disease pathogenesis and therapeutic response.

PROVIDER: EGAS00001004424 | EGA |

REPOSITORIES: EGA

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Novel methodology to discern predictors of remission and patterns of disease activity over time using rheumatoid arthritis clinical trials data.

RMD open 20181025 2

<h4>Objectives</h4>To identify predictors of remission and disease activity patterns in patients with rheumatoid arthritis (RA) using individual participant data (IPD) from clinical trials.<h4>Methods</h4>Phase II and III clinical trials completed between 2002 and 2012 were identified by systematic literature review and contact with UK market authorisation holders. Anonymised baseline and follow-up IPD from <i>non-biological arms</i> were amalgamated. Multiple imputation was used to handle missi ...[more]

PMID: 30487994

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RA-MAP: mapping molecular immunological landscapes in early rheumatoid arthritis and healthy vaccine recipients [Healthy Hepatitis B Vaccine Recipients]

Project description:Rheumatoid arthritis (RA) is a chronic inflammatory disorder with poorly defined aetiology characterised by synovial inflammation with variable disease severity and drug responsiveness. To investigate the peripheral blood immune cell landscape of RA, we performed comprehensive clinical and molecular profiling of 267 RA patients and 52 vaccine recipient controls for up to 18 months to establish a high quality sample biobank including plasma, serum, peripheral blood cells, urine, genomic DNA, RNA from whole blood, lymphocyte and monocyte subsets. We have performed extensive multi-omic immune phenotyping, including genomic, metabolomic, proteomic, transcriptomic and autoantibody profiling. We anticipate that these detailed clinical and molecular data will serve as a fundamental resource offering insights into disease pathogenesis, progression and therapeutic response, ultimately contributing to the development and application of targeted therapies for RA.

2021-05-12 | GSE97475 | GEO

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RA-MAP: mapping the molecular immunological landscape in early rheumatoid arthritis with vaccine controls

Project description:<p>Rheumatoid arthritis (RA) is a chronic inflammatory disorder with poorly defined aetiology characterised by synovial inflammation with variable disease severity and drug responsiveness. To investigate the peripheral blood immune cell landscape of RA, we performed comprehensive clinical and molecular profiling of 267 RA patients and 52 healthy vaccine recipients for up to 18 months to establish a high quality sample biobank including plasma, serum, peripheral blood cells, urine, genomic DNA, RNA from whole blood, lymphocyte and monocyte subsets. We have performed extensive multi-omic immune phenotyping, including genomic, metabolomic, proteomic, transcriptomic and autoantibody profiling. We anticipate that these detailed clinical and molecular data will serve as a fundamental resource offering insights into immune-mediated disease pathogenesis, progression and therapeutic response, ultimately contributing to the development and application of targeted therapies for RA.</p>

2021-06-16 | MTBLS1497 | MetaboLights

RA-MAP: mapping molecular immunological landscapes in early rheumatoid arthritis and healthy vaccine recipients

Project description:RA-MAP: mapping molecular immunological landscapes in early rheumatoid arthritis and healthy vaccine recipients

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Comparison of gene expression profiles in paired synovial biopsies from rheumatoid arthritis (RA) patients

Project description:We explored transcriptomic profiles of paired synovial biopsies from RA patients, in order to assess heterogeneity in synovial tissue at the individual level. Pairwise comparison of transcriptomic profiles showed similar expression of RA-related molecular pathways (TCR signaling, T cell co-stimulation and response to TNF⍺), thereby showing that global molecular alterations in RA synovitis are similar between small and large joints from the same patient.

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CGH analysis of Rheumatoid arthritis (RA) patient genomes

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.

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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by TL1A

Project description:TNF-like ligand 1A (TL1A) is a member of TNF receptor superfamily and involved in the pathogenesis of autoimmune diseases including rheumatoid arthritis (RA) by inducing apoptosis via intracellular death domain or promoting inflammation through the activation of NFκB by binding to its specific receptor death receptor 3 (DR3). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble TL1A in addition to Fas-ligand (FasL) and LIGHT and inhibits the signaling of TL1A via DR3. Therefore, TL1A-DcR3/DR3 signaling may be involved in the pathogenesis of RA by modulating apoptosis and proliferation of RA-FLS. We hypothesized that TL1A regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by TL1A.

2018-08-24 | GSE118958 | GEO

Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by FasL

Project description:Fas ligand (FasL)/TNFSF6, a member of the tumor necrosis factor (TNF) superfamily, can promote apoptosis in activated primary B cells, T cells, dendritic cells, and synovial fibroblasts through Fas and is involved in the pathogenesis of autoimmune diseases including rheumatoid arthritis (RA). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble FasL in addition to TL1A and LIGHT and inhibits the signaling of FasL via Fas. Therefore, FasL-DcR3/Fas signaling may be involved in the pathogenesis of RA. We hypothesized that FasL regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by FasL.

2020-06-30 | GSE153378 | GEO

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