Search results for: TLR3 TLR3.7
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Oncolytic Reovirus Inhibits Immunosuppressive Activity of Myeloid-Derived Suppressor Cells in a TLR3-Dependent Manner.Oncolytic reovirus, which possesses 10 segments of dsRNA genome, mediates antitumor effects via not only virus replication in a tumor cell-specific manner, but also activation of antitumor immunity; however, the mechanism(s) of reovirus-induced activation of antitumor immunity have not been fully elucidated. Recent studies have demonstrated that overcoming an immunosuppressive environment in tumor-bearing hosts is important to achieve efficient activation of antitumor immunity. Among the various types of cells involved in immunosuppression, it has been revealed that myeloid-derived suppressor cells (MDSCs) are significantly increased in tumor-bearing hosts and play crucial roles in the immunosuppression in tumor-bearing hosts. In this study, we examined whether reovirus inhibits the immunosuppressive activity of MDSCs, resulting in efficient activation of immune cells after in vivo administration. The results showed that splenic MDSCs recovered from PBS-treated tumor-bearing mice significantly suppressed the Ag-specific proliferation of CD8T cells. In contrast, the suppressive activity of MDSCs on T cell proliferation was significantly reduced after reovirus administration. Reovirus also inhibited the immunosuppressive activity of MDSCs in IFN-β promoter stimulator-1 knockout (KO) mice and in wild-type mice. In contrast, the immunosuppressive activity of MDSCs in TLR-3 KO mice was not significantly altered by reovirus treatment. The activation levels of CD4and CD8T cells were significantly lower in TLR3 KO mice than in wild-type mice after reovirus administration. These results indicate that reovirus inhibits the immunosuppressive activity of MDSCs in a TLR3, but not IFN-β promoter stimulator-1, signaling-dependent manner.
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STATUS OF THE SYSTEM OF SIGNALING PATTERN RECOGNITION RECEPTORS OF MONOCYTES AND GRANULOCYTES IN COSMONAUTS' PERIPHERAL BLOOD BEFORE AND AFTER LONG-DURATION MISSIONS TO THE INTERNATIONAL SPACE STATION.The system of signaling pattern recognition receptors was studied in 8 cosmonauts aged 35 to 56 years before and after (R+) long-duration missions to the International space station. Peripheral blood samples were analyzed for the content of monocytes and granulocytes that express the signaling pattern recognition Toll- like (TLR) receptors localized as on cell surface (TLR1, TLR2, TLR4, TLR5, TLR6), so inside cells (TLR3, TLR8, TLR9). In parallel, serum concentrations of TLR2 (HSP60) and TLR4 ligands (HSP70, HMGB1) were measured. The results of investigations showed growth of HSP60, HSP70 and HMGB1 concentrations on R+1. In the;majority of cosmonauts increases in endogenous ligands were followed by growth in the number of both monocytes and granulocytes that express TLR2 1 TLR4. This consistency gives ground to assume that changes in the system of signaling pattern recognition receptors can stem .from the predominantly endogenous ligands' response to the effects of long-duration space flight on human organism.
1390 related Products with: STATUS OF THE SYSTEM OF SIGNALING PATTERN RECOGNITION RECEPTORS OF MONOCYTES AND GRANULOCYTES IN COSMONAUTS' PERIPHERAL BLOOD BEFORE AND AFTER LONG-DURATION MISSIONS TO THE INTERNATIONAL SPACE STATION.FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Thermal Shaker with cooli FDA Standard Frozen Tissu FDA Standard Frozen Tissu Ofloxacin CAS Number [824 Multiple organ tumor tiss MultiGene Gradient therm BACTERIOLOGY BACTEROIDES REASTAIN® Quick Diff Kit
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Integrated analysis of microarray data to identify the genes critical for the rupture of intracranial aneurysm.Intracranial aneurysm (IA) is a localized dilation of the blood vessel. The present study was designed to explore the mechanisms of rupture of IA. GSE13353 (including 11 ruptured and 8 unruptured IA samples) and GSE15629 (including 8 ruptured and 6 unruptured IA samples) were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) identified using limma and MetaDE packages were merged, and a protein-protein interaction (PPI) network analysis was performed using Cytoscape software. Pathway enrichment analysis was performed for the nodes of the PPI network using the fisher algorithm. The 100 most prominent genes in the network were designated candidate genes and a hierarchical clustering analysis was performed. The tune.svm function of e1071 package was used to construct a support vector machine (SVM) classifier, and the Candidate Cancer Gene Database was applied to analyze the characterization of gene-associated cancer. Furthermore, the genes involved in the SVM classifier were assessed via principal component analysis (PCA). In the ruptured samples, 1,292 DEGs and 1,029 DEGs separately were identified by limma and MetaDE packages. The 100 most prominent genes in the network included fibronectin 1 (FN1), amyloid β (A4) precursor protein (APP), nuclear RNA export factor 1 (NXF1) and signal transducer and activator of transcription 3 (STAT3). Pathway enrichment analysis identified that toll-like receptor 3 (TLR3) was enriched in the Toll-like receptor signaling pathway. A total of 15 genes (including FN1) were used to construct the SVM classifier. NXF1 was identified to be associated with Nervous System Cancer. PCA revealed that APP, NXF1 and STAT3 were the 3 principal components. TLR3, FN1, APP, NXF1 and STAT3 may affect the rupture of IA.
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Pathways of airway oxidant formation by house dust mite allergens and viral RNA converge through myosin motors, pannexons and Toll-like receptor 4.Intracellular reactive oxidant species (ROS) are generated in human airway epithelial cells by the prothrombinase action of Group 1 house dust mite (HDM) allergens and by ligation of viral RNA sensor Toll-like receptors (TLRs). We explored signaling convergence between HDM allergens and TLRs in ROS generation because epithelial cells form the primary barrier against inhaled substances and dictate host responses to allergens and viruses.
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P2YReceptors Regulate CXCL10 Expression and Secretion in Mouse Intestinal Epithelial Cells.In this study, we investigated the role of extracellular nucleotides in chemokine (KC, MIP-2, MCP-1, and CXCL10) expression and secretion by murine primary intestinal epithelial cells (IECs) with a focus on P2Yreceptors. qRT-PCR experiments showed that P2Ywas the dominant nucleotide receptor expressed in mouse IEC. In addition, the P2Yligand UDP induced expression and secretion of CXCL10. For the other studies, we took advantage of mice deficient in P2Y(). Similar expression levels of P2Y, P2Y, P2X2, P2X4, and Awere detected inand WT IEC. Agonists of TLR3 (poly(I:C)), TLR4 (LPS), P2Y, and P2Yincreased the expression and secretion of CXCL10 more prominently inIEC than in WT IEC. CXCL10 expression and secretion induced by poly(I:C) in bothand WT IEC were inhibited by general P2 antagonists (suramin and Reactive-Blue-2), by apyrase, and by specific antagonists of P2Y, P2Y, P2Y(only in WT), and P2X4. Neither adenosine nor an Aantagonist had an effect on CXCL10 expression and secretion. Macrophage chemotaxis was induced by the supernatant of poly(I:C)-treated IEC which was consistent with the level of CXCL10 secreted. Finally, the non-nucleotide agonist FGF2 induced MMP9 mRNA expression also at a higher level inIEC than in WT IEC. In conclusion, extracellular nucleotides regulate CXCL10 expression and secretion by IEC. In the absence of P2Y, these effects are modulated by other P2 receptors also present on IEC. These data suggest that the presence of P2Yregulates chemokine secretion and may also regulate IEC homeostasis.
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Intravesicular Acidification Regulates Lipopolysaccharide Inflammation and Tolerance through TLR4 Trafficking.TLRs recognize pathogen components and drive innate immune responses. They localize at either the plasma membrane or intracellular vesicles such as endosomes and lysosomes, and proper cellular localization is important for their ligand recognition and initiation of signaling. In this study, we disrupted ATP6V0D2, a component of vacuolar-type Hadenosine triphosphatase (V-ATPase) that plays a central role in acidification of intracellular vesicles, in a macrophage cell line. ATP6V0D2-deficient cells exhibited reduced cytokine production in response to endosome-localized, nucleic acid-sensing TLR3, TLR7, and TLR9, but enhanced inflammatory cytokine production and NF-κB activation following stimulation with LPS, a TLR4 agonist. Moreover, they had defects in internalization of cell surface TLR4 and exhibited enhanced inflammatory cytokine production after repeated LPS stimulation, thereby failing to induce LPS tolerance. A component of the V-ATPase complex interacted with ARF6, the small GTPase known to regulate TLR4 internalization, and ARF6 deficiency resulted in prolonged TLR4 expression on the cell surface. Taken together, these findings suggest that ATP6V0D2-dependent intravesicular acidification is required for TLR4 internalization, which is associated with prevention from excessive LPS-triggered inflammation and induction of tolerance.
2658 related Products with: Intravesicular Acidification Regulates Lipopolysaccharide Inflammation and Tolerance through TLR4 Trafficking.TLR4 Androgen Receptor (Phosph Androgen Receptor (Phosph Mouse Anti-Chlamydia Lipo Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Human lipopolysaccharide( TLR4 Antibody TLR4 Antibody TLR4 Blocking Peptide AZD-3514 Mechanisms: Andr
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Role of Toll-like receptors and interferon regulatory factors in different experimental heart failure models of diverse etiology: IRF7 as novel cardiovascular stress-inducible factor.Heart failure (HF) is a leading cause of morbidity and mortality in the western world. Although optimal medical care and treatment is widely available, the prognosis of patients with HF is still poor. Toll-like receptors (TLRs) are important compartments of the innate immunity. Current studies have identified TLRs as critical mediators in cardiovascular diseases. In the present study, we investigated the involvement of TLRs and interferon (IFN) regulatory factors (IRFs) in different experimental HF models including viral myocarditis, myocardial ischemia, diabetes mellitus, and cardiac hypertrophy. In addition, we investigated for the first time comprehensive TLR and IRF gene and protein expression under basal conditions in murine and human cardiac tissue. We found that Tlr4, Tlr9 and Irf7 displayed highest gene expression under basal conditions, indicating their significant role in first-line defense in the murine and human heart. Moreover, induction of TLRs and IRFs clearly differs between the various experimental HF models of diverse etiology and the concomitant inflammatory status. In the HF model of acute viral-induced myocarditis, TLR and IRF activation displayed the uppermost gene expression in comparison to the remaining experimental HF models, indicating the highest amount of myocardial inflammation in myocarditis. In detail, Irf7 displayed by far the highest gene expression during acute viral infection. Interestingly, post myocardial infarction TLR and IRF gene expression was almost exclusively increased in the infarct zone after myocardial ischemia (Tlr2, Tlr3, Tlr6, Tlr7, Tlr9, Irf3, Irf7). With one exception, Irf3 showed a decreased gene expression in the remote zone post infarction. Finally, we identified Irf7 as novel cardiovascular stress-inducible factor in the pathologically stressed heart. These findings on TLR and IRF function in the inflamed heart highlight the complexity of inflammatory immune response and raise more interesting questions for future investigation.
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Transcriptional Innate Immune Response of the Developing Chicken Embryo to Newcastle Disease Virus Infection.Traditional approaches to assess the immune response of chickens to infection are through animal trials, which are expensive, require enhanced biosecurity, compromise welfare, and are frequently influenced by confounding variables. Since the chicken embryo becomes immunocompetent prior to hatch, we here characterized the transcriptional response of selected innate immune genes to Newcastle disease virus (NDV) infection in chicken embryos at days 10, 14, and 18 of embryonic development. The results suggest that the innate immune response 72 h after challenge of 18-day chicken embryo is both consistent and robust. The expression of CCL5, Mx1, and TLR3 in lung tissues of NDV challenged chicken embryos from the outbred Kuroiler and Tanzanian local ecotype lines showed that their expression was several orders of magnitude higher in the Kuroiler than in the local ecotypes. Next, the expression patterns of three additional innate-immunity related genes, IL-8, IRF-1, and STAT1, were examined in the highly congenic Fayoumi (M5.1 and M15.2) and Leghorn (Ghs6 and Ghs13) sublines that differ only at the microchromosome bearing the major histocompatibility locus. The results show that the Ghs13 Leghorn subline had a consistently higher expression of all genes except IL-8 and expression seemed to be subline-dependent rather than breed-dependent, suggesting that the innate immune response of chicken embryos to NDV infection may be genetically controlled by the MHC-locus. Taken together, the results suggest that the chicken embryo may represent a promising model to studying the patterns and sources of variation of the avian innate immune response to infection with NDV and related pathogens.
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Secretion of Hepatitis C Virus Replication Intermediates Reduces Activation of Toll Like Receptor 3 in Hepatocytes.Hepatitis C virus (HCV) infections most often result in chronic outcomes, although the virus constantly produces replication intermediates, in particular double-stranded RNA (dsRNA), representing potent inducers of innate immunity. We aimed to characterize the fate of HCV dsRNA in hepatocyte cultures to identify mechanisms contributing to viral persistence in presence of an active innate immune response.
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Potential mediators of in ovo delivered double stranded (ds) RNA-induced innate response against low pathogenic avian influenza virus infection.Toll like receptor (TLR) 3 is a critically important innate pattern recognizing receptor that senses many viral infections. Although, it has been shown that double stranded (ds) RNA can be used for the stimulation of TLR3 signaling pathway in a number of host-viral infection models, it's effectiveness as an antiviral agent against low pathogenic avian influenza virus (LPAIV) needs further investigation.
1805 related Products with: Potential mediators of in ovo delivered double stranded (ds) RNA-induced innate response against low pathogenic avian influenza virus infection.Avian Influenza Virus H5N Avian Influenza virus H5N Avian Influenza virus (H7 Avian Influenza virus H5N Avian Influenza virus H5N Influenza virus A&B Real Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Mouse Epstein-Barr Virus
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