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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE118958 | GEO | 2018/08/24

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 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 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 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 DcR3

2013-04-02 | GSE45665 | 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

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

The effects of knockout TL1A on LPS-induced ARDS mice

Project description:The TNF superfamily is large, including TNF ligands (n = 19) and TNF receptors (n = 29),as determined following the completion of large-scale sequencing of the human and mouse genomes. These members not only function in immune cells but are also involved in respiratory and intestinal diseases, and some members may act as a double-edged sword. Tumor necrosis factor-like cytokine 1A (TL1A, also known as TNFSF15) is the only known death receptor 3 (DR3, also known as TNFRSF25) ligand (Meylan et al., 2011). The TL1A/DR3 axis plays a role in the regulation of intestinal immunity and fibrosis (Valatas et al., 2019), asthma airway remodeling (Zhang et al., 2022; Herro et al., 2010), and other autoimmune and inflammatory diseases (Herro et al., 2021), exacerbating disease progression. However, some researchers have proposed that the TL1A/DR3 axis has a protective role in some disease models. A novel role for TL1A/DR3 in protection against intestinal injury was reported by Jia et al (Jia et al., 2016). Yang et al. revealed a protective effect of TL1A against intracerebral hemorrhage-induced secondary brain injury and infection (Yang et al., 2021). In addition, TL1A maintains the blood–retinal barrier by modulating SHP-1-Src-VE-cadherin signaling in diabetic retinopathy, as verified by Li et al (Li et al., 2021). However, the role of TL1A/DR3 in ARDS has not been explored.

2023-02-07 | PXD039909 | iProX

Differences in proteins between normal and asthmatic mice and effects of knockout TL1A on asthmatic mice

Project description:Asthma, a heterogeneous disease, is characterized by chronic inflammation, epithelial–mesenchymal transformation (EMT), and airway remodeling. After immune system activation, macrophages, T cells, and other cells gather and secrete various factors, such as interleukin-1β, 4, 5, 10, 13, and TNF-a, which break the anti-inflammatory balance and aggravate the progression of asthma. TNF-a, a member of the TNF superfamily, has promising future in the pathophysiological progress of autoimmune diseases and the development and application of related drugs. However, the mechanisms of TNF-a in mucus secretion, airway hyperreactivity, and airway remodeling of human asthma remains unclear. Tumor necrosis factor-like cytokine 1A is a type II transmembrane protein with a stable trimer structure similar to TNF-a. Migone et al. first uncovered the presence of TL1A as a membrane-bound protein (mTL1A) or a soluble protein (sTL1A) from mTL1A cleaved by an underlying enzyme. DR3 is a type I membrane protein that contains a death domain in the cytoplasmic region and remains highly homologous with other TNFRSF members. Interestingly, Evangelos et al. found that TNF-a-stimulated human lung myofibroblasts significantly increase TL1A expression and collagen production. Our study will identify the specific role of TNF-a-stimulated mTL1A/DR3 or sTL1A/DR3 axis in the EMT of asthma model.

2022-05-20 | PXD031079 | Pride

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

Gene expression from fibroblast-like synoviocytes (FLS) of three patients with rheumatoid arthritis (RA) that were cultured in four conditions: control medium (Basal), ATRA, TNF and ATRA+TNF.

Project description:The aim of this study was to investigate the response of FLS from RA patients to retinoic acid and retinoic acid combined with the central cytokine of RA, TNF.

2019-12-09 | GSE120785 | GEO

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