Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene profiling in the colon after depletion and activation of TLR3 and TLR7 signals

ABSTRACT: TLR3 and TLR7 are critical recognition receptor which reacts with viruses. TLR3 and TLR7 contribute to many immunological pathway. Especially, TLR3 and TLR7 are clearly involved in the regulation of innate immunity in the gut. To identify the downstream target of TLR 3 and TLR7 in the IBD, we carried out microarray.

ORGANISM(S): Mus musculus

PROVIDER: GSE79241 | GEO | 2016/07/05

SECONDARY ACCESSION(S): PRJNA315269

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene profiling in the colon after depletion and activation of TLR3 and TLR7 signals

Project description:TLR3 and TLR7 are critical recognition receptor which reacts with viruses. TLR3 and TLR7 contribute to many immunological pathway. Especially, TLR3 and TLR7 are clearly involved in the regulation of innate immunity in the gut. To identify the downstream target of TLR 3 and TLR7 in the IBD, we carried out microarray. The colon tissues were isolated from four different groups. None-no treatment, after DSS treated, after DSS+antiviral treatment, after DSS+TLR3+7 agonists.

2016-07-05 | E-GEOD-79241 | biostudies-arrayexpress

TLR3, TLR7, and TLR9 stimulation in murine dorsal root ganglion neurons

Project description:TLR3, TLR7, and TLR9 stimulation induces many mouse inflammatory and autoimmune cytokines or immune receptors

2011-03-02 | GSE27579 | GEO

TLR3, TLR7, and TLR9 stimulation in murine dorsal root ganglion neurons

Project description:TLR3, TLR7, and TLR9 stimulation induces many mouse inflammatory and autoimmune cytokines or immune receptors DRGN were cultures 5 days prior to a 16 hour stimulation - Three separate studies were analyzed for inflammatory response

2011-03-02 | E-GEOD-27579 | biostudies-arrayexpress

UNC93B1 variants underlie TLR7-dependent autoimmunity

Project description:UNC93B1 is critical for trafficking and function of nucleic acid-sensing Toll-like receptors (TLRs) TLR3, TLR7, TLR8, and TLR9, which are essential for antiviral immunity. Overactive TLR7 signaling induced by recognition of self-nucleic acids has been implicated in systemic lupus erythematosus (SLE). Here, we report UNC93B1 variants (E92G and R336L) in four patients with early-onset SLE. Patient cells or mouse macrophages carrying the UNC93B1 variants produced high amounts of TNF-α and IL-6 and upon stimulation with TLR7/TLR8 agonist, but not with TLR3 or TLR9 agonists. E92G causes UNC93B1 protein instability and reduced interaction with TLR7, leading to selective TLR7 hyperactivation with constitutive type I IFN signaling. Thus, UNC93B1 regulates TLR subtype-specific mechanisms of ligand recognition. Our findings establish a pivotal role for UNC93B1 in TLR7-dependent autoimmunity and highlight the therapeutic potential of targeting TLR7 in SLE.

2023-12-14 | GSE250223 | GEO

Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3 and TLR7 activation in Bone-marrow-derived macrophage

Project description:The goal of this study is to compare gene expression between TLR3 and TLR7

2021-05-14 | GSE163347 | GEO

Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3, TLR7 and TLR8 Activation in Neurons

Project description:The goal of this study is to compare gene expression of mouse cultured cortical and hippocampal neurons in response to TLR3, TLR7 and TLR8 activation

2018-05-15 | GSE107199 | GEO

Dysregulated TLR7 signaling drives anemia via development of hemophagocytic macrophages

Project description:The debilitating autoimmune disease Systemic Lupus Erythematosus (SLE) is closely associated with Toll-like receptor (TLR) 7 and type I interferon (IFN) activity in humans and in murine SLE-like disease. Two central manifestations of SLE affect the myeloid lineage of the immune system, myeloid expansion and anemia. Yet, whether these symptoms are linked and the role of TLR7 and/or type I IFN in these processes is unclear. Here we show that TLR7 signaling promotes cell-autonomous, phosphoinositide 3-kinase (PI3K)- and mammalian target of rapamycin (mTOR)-dependent macrophage development from the common myeloid progenitor (CMP). Strikingly, this TLR7-driven macrophage development requires and is enhanced by type I IFN. Genome-wide transcriptional profiling and functional studies demonstrated that TLR7 promoted the expression of Spic, the master regulator of splenic red pulp macrophages (RPM) and preferential development of hemophagocytic RPM-like cells from CMP in vitro. We found increased incidence of RPM-like cells in vivo in a mouse model of SLE caused by TLR7 overexpression, which correlated with decreased red blood cell (RBC) count and anemia. These findings demonstrate a mechanism by which TLR7 signaling promotes anemia that is of clinical significance in SLE, other rheumatological diseases and chronic viral infections. This work also identifies a previously unknown molecular pathway by which TLR signaling and type I IFN synergize to promote myeloid development from hematopoietic progenitors. CMP were sorted from the bone marrow of wild-type C57BL/6 mice, cultured with SCF+R848 or SCFr+MCSF, and CD11b+F4/80+ macrophages sorted after 5 days, n=3 per group

2016-07-01 | E-GEOD-70520 | biostudies-arrayexpress

Bruton's Tyrosine Kinase Regulates TLR9 but not TLR7 Signaling in Human pDCs

Project description:Plasmacytoid dendritic cells (pDCs) can be activated by the endosomal TLRs, and contribute to the pathogenesis of systemic lupus erythematosus (SLE) by producing type I IFNs. Thus, blocking TLR-mediated pDC activation may represent a useful approach for the treatment of SLE. In an attempt to identify a therapeutic target for blocking TLR signaling in pDCs, we investigated the contribution of Bruton's tyrosine kinase (Btk) to the activation of pDCs by TLR7 and TLR9 stimulation by using a selective Btk inhibitor RN486. Stimulation of TLR7 and 9 with their respective agonist, namely, gardiquimod and type A CpG ODN2216, resulted in the activation of human pDCs, as demonstrated by the expression of activation markers (CD69, CD40, and CD86), elevated production of IFN-alpha and other inflammatory cytokines, as well as up-regulation of numerous genes including IFN-alpha-inducible genes and activation of interferon regulatory factor 7 (IRF7) and NF-kB. RN486 inhibited all of these events induced by TLR9, but not TLR7 stimulation, with a nanomolar potency for inhibiting type A CpG ODN2216-mediated production of cytokines (e.g., IC50=386 nM for inhibiting IFN-alpha). Our data reveal Btk as an important regulatory enzyme in the TLR9 pathway, and a potential therapeutic target for SLE and other TLR-driven diseases. pDCs from healthy donors (n=4) were treated with gardiquimod (TLR7 agonist) or ODN 2216 (TLR9 agonist) with or without BTK inhibitor for 3 hours.

2015-10-24 | E-GEOD-41825 | biostudies-arrayexpress

TLR signaling in C57BL/6J TLR7-tolerant CD3+ T-cells over B6 TLR7 null CD3+ T-cells.

Project description:Murine CD3+ T-cells were immunomagnetically purified from the spleens of C57BL/6J mice and were pretreated in vitro for three days in the presence of R848 (5 μg/ml). Gene expression profile of wild type (WT) C57BL/6J TLR7-primed T-cells, was compared to unmanipulated B6 TLR7 null CD3+ Τ-cells. We used Qiagen Toll-like Receptor RT2 Profiler PCR Array kit to quantitate gene expression profiling of the TLR signaling pathway.

2017-04-21 | GSE80573 | GEO

Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3, TLR7 and TLR8 Activation in Neurons

Project description:Next Generation Sequencing for Quantitative Transcriptomic Profiling of TLR3, TLR7 and TLR8 Activation in Neurons

| PRJNA419291 | ENA