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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by DcR3

ABSTRACT: Decoy receptor 3 (DcR3), a member of the tumor necrosis factor receptor (TNFR) superfamily, competitively binds and inhibits members of the TNF family, including Fas ligand (FasL), LIGHT, and TL1A. DcR3 was recently reported not only to act as a decoy receptor for these TNFRs but also to play a role as a ligand for the pathogenesis of RA. We hypothesized that DcR3 regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by the ligation of DcR3.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45665 | GEO | 2013/04/02

SECONDARY ACCESSION(S): PRJNA195568

REPOSITORIES: GEO

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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by DcR3

Project description:Decoy receptor 3 (DcR3), a member of the tumor necrosis factor receptor (TNFR) superfamily, competitively binds and inhibits members of the TNF family, including Fas ligand (FasL), LIGHT, and TL1A. DcR3 was recently reported not only to act as a decoy receptor for these TNFRs but also to play a role as a ligand for the pathogenesis of RA. We hypothesized that DcR3 regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by the ligation of DcR3. RA-FLS were obtained from 4 RA patients (sample1-4). Each sample was incubated with control IgG1 or human DcR3-Fc. Gene expression in RA-FLS stimulated by DcR3-Fc was compared with that of their respective unstimulated controls.

2013-04-02 | E-GEOD-45665 | biostudies-arrayexpress

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 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. DcR3 overexpressed in rheumatoid synovial fibroblasts (RA-FLS) stimulated with inflammatory cytokines such as TNFα or IL-1β inhibits Fas-induced apoptosis. In contrast, DcR3 inhibited cell proliferation induced by inflammatory cytokines via membrane-bound TL1A expressed on RA-FLS. 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 the ligation of TL1A.

2014-12-10 | GSE63995 | GEO

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 TL1A

Project description:TNF-like ligand 1A (TL1A) is a member of TNF receptor superfamily and involved in the pathogenesis of autoimmune diseases by inducing apoptosis via intracellular death domain or promoting inflammation through the activation of NFM-NM-:B 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. DcR3 overexpressed in rheumatoid synovial fibroblasts (RA-FLS) stimulated with inflammatory cytokines such as TNFM-NM-1 or IL-1M-NM-2 inhibits Fas-induced apoptosis. In contrast, DcR3 inhibited cell proliferation induced by inflammatory cytokines via membrane-bound TL1A expressed on RA-FLS. 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 the ligation of TL1A. RA-FLS were obtained from 4 RA patients (sample1-4). Each sample was incubated with either 1.0 M-NM-<g/ml recombinant human TL1A protein or phosphate buffered saline (PBS) diluted with serum-free Opti-MEM medium as non-stimulated control for 12 hours at 37M-BM-0C with 5% CO2. Gene expression in RA-FLS stimulated by TL1A was compared with that of their respective non-stimulated controls.

2014-12-10 | E-GEOD-63995 | biostudies-arrayexpress

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

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

Project description:LIGHT/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 LIGHT in addition to TL1A and FasL and inhibits the signaling of LIGHT via HEVN and. Therefore, LIGHT-DcR3/HEVN/ signaling may be involved in the pathogenesis of RA. We hypothesized that LIGHT regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by LIGHT.

2022-02-20 | GSE197057 | GEO

Identification of genes regulating TRAIL-induced apoptosis in rheumatoid arthritis fibroblasts-like synoviocytes (RA FLS)

Project description:Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease involving primarily the synovial membranes and articular structures of multiple joints. A hallmark of RA is the pseudo-tumoral expansion of fibroblast-like synoviocytes (FLS), as these cells invade and finally destroy the joint structure. RA FLS have been therefore proposed as a therapeutic target. > TNF-related apoptosis-inducing ligand (TRAIL) has been described as a pro-apoptotic factor on malignant cells. The fact that fibroblasts-like-synoviocytes (FLS) in rheumatoid arthritis RA patients exhibit tumor like features led us to investigate the effect of TRAIL on ex-vivo RA FLS. We have previously described that TRAIL induces apoptosis only in a subset of RA FLS, but an induction of proliferation in the surviving cells. This observation corresponds to the pleiotropic effects of TRAIL observed on primary human tumor cells. We also observed that sensitivity to TRAIL-induced apoptosis varied in RA FLS from one patient to another, and was correlated with disease severity. We therefore screened for genes that were differentially expressed in RA FLS sensitive and resistant to TRAIL induced apoptosis in order to understand molecular factors making cells resistant or sensitive to TRAIL induced apoptosis.

2018-02-12 | GSE65908 | GEO

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

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

| PRJNA642862 | ENA

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

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

| PRJNA487531 | ENA

Transcription profiling by array of human monocytes were cultured with DcR3 in the presence of M-CSF

Project description:Decoy receptor 3 (DcR3) is a member of the TNF receptor superfamily and is up-regulated in tumors that originate from a diversity of lineages. DcR3 is capable of promoting angiogenesis, inducing dendritic cell apoptosis, and modulating macrophage differentiation. Since tumor-associated macrophages (TAMs) are the major infiltrating leukocytes in most malignant tumors, we used microarray technology to investigate whether DcR3 contributes to the development of TAMs. Among the DcR3-modulated genes expressed by TAMs, those that encode proteins involved in MHC class II (MHC-II)-dependent antigen presentation were down-regulated substantially, together with the master regulator of MHC-II expression (the class II transactivator, CIITA). The ERK- and JNK-induced deacetylation of histones associated with the CIITA promoters was responsible for DcR3-mediated down-regulation of MHC-II expression. Furthermore, the expression level of DcR3 in cancer cells correlated inversely with HLA-DR levels on TAMs and with the overall survival time of pancreatic cancer patients. The role of DcR3 in the development of TAMs was further confirmed using transgenic mice over-expressing DcR3. This elucidates the molecular mechanism of impaired MHC-II-mediated antigen presentation by TAMs, and raises the possibility that subversion of TAM-induced immunosuppression via inhibition of DcR3 expression might represent a target for the design of new therapeutics. Experiment Overall Design: Freshly isolated human monocytes were cultured with DcR3 or control hIgG1 in the presence of M-CSF for 2 days. Data were collected from two independent donors

2008-04-05 | E-GEOD-10856 | biostudies-arrayexpress

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