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Transcriptional profile of TL1A transgenic mice

ABSTRACT: To assess the effect of different forms of TL1A within different organs of the mouse we generated 2 different transgenic mouse lines where TL1A was expressed under the control of the CD2 promoter. 2 forms of TL1A was used. Either WT TL1A, which led to over expression of both membrane bound and soluble forms of TL1A (Refered to as Mem+Sol) or TL1A Delta 69-93 which only overexpressed membrane restricted TL1A (Refered to as Mem). Lungs and terminal ileums were taken from Either Mem, Mem+sol or WT litermate control mice at 12 weeks of age and the transcriptome assessed using RNAseq Through this we demonstrated enrichment of different transcripts and pathways both dependent on and independent of the form of TL1A and the site of action. This study is also the first to use RNASeq to assess the resualt of overexpression of TL1A within the mouse.

ORGANISM(S): Mus musculus

PROVIDER: GSE98492 | GEO | 2017/12/14

SECONDARY ACCESSION(S): PRJNA385261

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 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 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

The TNF family member TL1A induces IL-22 secretion in committed human TH17 cells via IL-9 induction

Project description:TL1A contributes to the pathogenesis of several chronic inflammatory diseases, including Inflammatory Bowel Diseases by enhancing TH1, TH17, and TH2 responses. TL1A mediates a strong co-stimulation of these TH subsets particularly of mucosal CCR9+ T cells. However, the signaling pathways that TL1A induces in different TH subsets are incompletely understood. Here, we investigated the function of TL1A on human TH17 cells. TL1A together with TGF- IL-6, and IL-23 enhanced the secretion of IL-17 and IFN- from human CD4+ memory T cells. TL1A induced the expression of the transcription factors BATF and T-bet that correlated with the secretion of IL-17 and IFN-. In contrast, TL1A alone induced high levels of IL-22 in memory CD4+ T cells and committed TH17 cells. However, TL1A did not enhance expression of IL-17A in TH17 cells. Expression of the transcription factor aryl hydrocarbon receptor that regulates expression of IL-22 was not affected by TL1A. We performed transcriptome analysis of TH17 cells to determine genes that are transcriptionally regulated by TL1A. transcriptome analysis revealed increased expression of IL-9 in response to TL1A.

2016-10-25 | GSE89133 | GEO

TL1A signaling enhances the differentiation of TH9 cells and TH9-driven mucosal pathologies via BATF and BATF3 signaling pathways

Project description:The TNF family member TL1A (TNFSF15) co-stimulates several T helper subsets and promotes T cell-dependent models of inflammatory diseases, including inflammatory bowel diseases (IBD) and allergic lung disease. TL1A polymorphisms confer susceptibility to IBD and have been associated with disease severity. In this study, we identified TL1A as a strong inducer of TH9 cell differentiation in vitro. Mechanistically, TL1A induced NF-B signaling and down-stream STAT6 activation and facilitated cooperative binding of BATF, BATF3, and IRF4 to the Il9 promoter. In vivo, utilizing an adoptive T cell transfer model we demonstrated that TL1A promoted IL-9-dependent, TH9 cell-induced intestinal and lung inflammation and blocking anti-IL-9 antibodies attenuated TL1A-driven mucosal inflammation. Our results demonstrate that TL1A promotes TH9 cell differentiation and function and define a role for IL-9 in TL1A-induced mucosal inflammation.

2019-01-08 | GSE60362 | GEO

TL1A is a central regulator of group 3 innate lymphoid cell function in colitis

Project description:Inflammatory bowel disease (IBD) results from a dysregulated interaction between the microbiota and a genetically susceptible host. Genetic studies have linked TNFSF15 polymorphisms and its protein TNF-like ligand 1A (TL1A) with IBD, but the functional role of TL1A in linking tissue homeostasis and intestinal inflammation is not known. Here, using cell-specific genetic deletion models, we report an essential role for CX3CR1+ mononuclear phagocyte (MNP)-derived TL1A, which is induced by adherent IBD-associated microbiota, in regulating group 3 innate lymphoid cell (ILC3) production of IL-22 and mucosal healing in acute colitis. However, in contrast to this protective role in acute colitis, TL1A-dependent expression of OX40L in MHCII+ ILC3 during colitis leads to co-stimulation of antigen-specific T cells and is required for chronic T cell colitis. These results identify a new role for ILC3 in regulating intestinal T cells and reveal a central role for TL1A in regulating ILC3 barrier immunity during colitis.

2018-12-26 | GSE120723 | 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

Proteome of group 2 innate lymphoid cells (ILC2s) stimulated with IL33 and TL1A

Project description:We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.

2024-03-05 | PXD041987 | Pride

Dissection of estrogen receptor alpha signaling pathways in osteoblasts using RNA-sequencing

Project description:The goal is to identify estrogen-dependent gene expression patterns using RNAseq for 3 different ERα forms in human osteoblasts. We analyzed 3 different forms of estrogen receptor alpha (ERα), 1) Wild-type, 2) NERKI (DNA-binding mutant) and 3) NOER (Nuclear Only ERα, not membrane). Each was infected into hFOB (human osteoblast) cells and treated with either vehicle or E2 (10nM) (n=3 for each group/treatment). RNAseq was then performed.

2015-03-11 | E-GEOD-55769 | biostudies-arrayexpress

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

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

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