Search results for "TLR3"

showing 10 items of 13 documents

1-ethyl-3-(6-methylphenanthridine-8-il) urea modulates TLR3/9 activation and induces selective pro-inflammatory cytokine expression in vitro.

2017

We have previously demonstrated the nucleic acid binding capacity of phenanthridine derivatives (PHTs). Because nucleic acids are potent inducers of innate immune response through Toll-like receptors (TLRs), and because PTHs bear a structural resemblance to commonly used synthetic ligands for TLR7/8, we hypothesized that PHTs could modulate/activate immune response. We found that compound M199 induces secretion of IL-6, IL-8 and TNFα in human PBMCs and inhibits TLR3/9 activation in different cellular systems (PBMCs, HEK293 and THP-1 cell lines).

0301 basic medicineClinical BiochemistryPharmaceutical ScienceDown-RegulationBiochemistryCell Line03 medical and health sciences0302 clinical medicineImmune systemDrug DiscoveryHumansImmunologic FactorsUreaSecretionReceptorMolecular BiologyInnate immune systemChemistryInterleukin-6Tumor Necrosis Factor-alphaOrganic ChemistryInterleukin-8Interferon-alphaTLR7Molecular biologyphenantridines ; TLR ; PBMCs ; cytokines ; immunomodulationIntercalating AgentsPhenanthridinesToll-Like Receptor 3030104 developmental biologyOligodeoxyribonucleotidesToll-Like Receptor 9TLR3Nucleic acidMolecular MedicineTumor necrosis factor alpha030215 immunologySignal TransductionBioorganicmedicinal chemistry letters
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Association of Toll-like receptors 2, 3, and 4 genes polymorphisms with periapical pathosis risk

2016

Background: The aim of this study was to investigate the role of gene variations of Toll-like receptors (TLR) 2, 3, and 4 on genetic susceptibility to periapical pathosis. Material and Methods: One hundred patients were included in the study and divided into two groups as follows; Control Group (n=50) that have root canal treatment and no periapical lesion, Patient Group (n=50) that have root canal treatment and periapical lesion. TLR2 Arg753Gln, TLR3 (c.1377C/T) and TLR4 Asp299Gly and Thr399Ile polymorphisms were genotyped by using PCR-RFLP. Genotypical analysis of control and patient groups were investigated to disclose whether there is any association between periapical lesions and gene …

0301 basic medicinePathologymedicine.medical_specialtyRoot canalOdontologíaGastroenterologyPolymorphism Single NucleotideEndodontics03 medical and health sciences0302 clinical medicineInternal medicineGenetic predispositionMedicineHumansGenetic Predisposition to DiseaseAlleleReceptorGeneral DentistryGeneAllelesOral Medicine and PathologyPolymorphism Geneticbusiness.industryResearchPeriapical DiseasesToll-Like ReceptorsPeriapical Pathosis030206 dentistry:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludToll-Like Receptor 2Toll-Like Receptor 3Toll-Like Receptor 4TLR2030104 developmental biologymedicine.anatomical_structureOtorhinolaryngologyCase-Control StudiesUNESCO::CIENCIAS MÉDICASTLR3TLR4SurgerybusinessMedicina Oral, Patología Oral y Cirugía Bucal
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Immunogenicity of a Fully Synthetic MUC1 Glycopeptide Antitumor Vaccine Enhanced by Poly(I:C) as a TLR3-Activating Adjuvant.

2017

Fully synthetic MUC1 glycopeptide antitumor vaccines have a precisely specified structure and induce a targeted immune response without suppression of the immune response when using an immunogenic carrier protein. However, tumor-associated aberrantly glycosylated MUC1 glycopeptides are endogenous structures, “self-antigens”, that exhibit only low immunogenicity. To overcome this obstacle, a fully synthetic MUC1 glycopeptide antitumor vaccine was combined with poly(inosinic acid:cytidylic acid), poly(I:C), as a structurally defined Toll-like receptor 3 (TLR3)-activating adjuvant. This vaccine preparation elicited extraordinary titers of IgG antibodies which strongly bound human breast cancer…

0301 basic medicinemedicine.medical_treatmentchemical and pharmacologic phenomenaBiochemistryCancer Vaccines03 medical and health sciencesMice0302 clinical medicineImmune systemCancer immunotherapyAdjuvants ImmunologicDrug DiscoverymedicineAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsMUC1PharmacologyVaccines SyntheticbiologyChemistryImmunogenicityOrganic ChemistryMucin-1GlycopeptidesDendritic CellsVirologyGlycopeptideToll-Like Receptor 3030104 developmental biologyPoly I-C030220 oncology & carcinogenesisTLR3biology.proteinMolecular MedicineAntibodyAdjuvantChemMedChem
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Toll-like receptors: Expression and involvement in Multiple Myeloma

2010

Multiple Myeloma (MM) cells express and respond to a broad range of TLRs. Accumulating evidences suggest that TLRs act as double-edged sword in MM biology. Indeed, TLR9 or TLR3 ligands could enhance immunity against MM cells or directly induce cell apoptosis, whereas various TLR agonists could induce MM survival, proliferation, and immune escape. This review is focused on the heterogeneous expression and function of TLRs in MM and on the potential implication of TLR ligands of infectious or endogenous origin in MM emergence, resistance, or progression.

Cancer ResearchTLR9ApoptosisEndogenyHematologyBiologyLigandsmedicine.diseaseToll-Like Receptor 3Cell biologyGene Expression Regulation NeoplasticImmune systemOncologyApoptosisImmunityToll-Like Receptor 9TLR3medicineAnimalsHumansTumor EscapeMultiple MyelomaReceptorMultiple myelomaLeukemia Research
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Toll-like receptor 3 mediates expression of clusterin/apolipoprotein J in vascular smooth muscle cells stimulated with RNA released from necrotic cel…

2010

Clusterin/Apolipoprotein J is a protein that is upregulated in a broad spectrum of diverse pathological processes. The predominant form is a secreted glycoprotein (sCLU) with cytoprotective and anti-inflammatory properties which shows enhanced expression in vascular smooth muscle cells (VSMC) following aortic injury and in atherosclerotic disease. Recent evidence indicates that during atherosclerosis, Toll-like receptors (TLRs) are activated in vascular cells by endogenous ligands. Here, we analyzed whether CLU expression in VSMC is controlled by TLRs, and stimulated by factors associated with or released by necrotic cells. Activation of TLR3 by the synthetic RNA analogue polyinosinic-polyc…

Cell ExtractsProtein DenaturationHot TemperatureMyocytes Smooth MuscleMedizinGene ExpressionBiologyTransfectionMuscle Smooth VascularCell LineMiceNecrosisDogsDownregulation and upregulationGene expressionAnimalsHumansChemokine CCL2Mice KnockoutMessenger RNAToll-like receptorClusterinToll-Like ReceptorsProteinsChloroquineCell BiologyMolecular biologyEndocytosisRatsToll-Like Receptor 3Mice Inbred C57BLTLR2Adaptor Proteins Vesicular TransportClusterinPoly I-CCulture Media ConditionedTLR3biology.proteinRNAEctopic expressionExperimental cell research
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TLR3-induced activation of mast cells modulates CD8+ T-cell recruitment.

2005

AbstractMast cells play an important role in host defense against various pathogens, but their role in viral infection has not been clarified in detail. dsRNA, synthesized by various types of viruses and mimicked by polyinosinic-polycytidylic acid (poly(I:C)) is recognized by Toll-like receptor 3 (TLR3). In this study, we demonstrate that poly(I:C) injection in vivo potently stimulates peritoneal mast cells to up-regulate a number of different costimulatory molecules. Therefore, we examined the expression and the functional significance of TLR3 activation in mast cells. Mast cells express TLR3 on the cell surface and intracellularly. After stimulation of mast cells with poly(I:C) and Newcas…

Chemokinevirusesmedicine.medical_treatmentImmunologyNewcastle disease virusReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesBiochemistryMicemedicineCytotoxic T cellAnimalsMast CellsPhosphorylationPeritoneal CavityMice KnockoutInnate immune systemMembrane GlycoproteinsToll-Like ReceptorsCell BiologyHematologymedicine.diseaseMast cellImmunity InnateCell biologyToll-Like Receptor 3Up-RegulationMice Inbred C57BLChemotaxis Leukocytemedicine.anatomical_structureCytokinePoly I-CTLR3ImmunologyMast cell sarcomabiology.proteinCytokinesCD8Blood
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Roflumilast improves corticosteroid resistance COPD bronchial epithelial cells stimulated with toll like receptor 3 agonist

2015

Chronic obstructive pulmonary disease (COPD) is characterised by chronic pulmonary inflammation punctuated by periods of viral exacerbations. Recent evidence suggests that the combination of roflumilast with corticosteroids may improve the compromised anti-inflammatory properties of corticosteroids in COPD. We analyzed differential and combination anti-inflammatory effects of dexamethasone and roflumilast N-oxide in human bronchial epithelial cells (HBECs) stimulated with viral toll like receptor (TLR) agonists. Lung tissue and HBECs were isolated from healthy (n = 15), smokers (n = 12) and smokers with COPD (15). TLR3 expression was measured in lung tissue and in HBECs. IL-8 secretion was …

CyclopropanesMaleAnti-Inflammatory AgentsDrug ResistanceAminopyridinesDexamethasonePulmonary Disease Chronic ObstructiveRoflimilastAdrenal Cortex HormonesToll like receptorsCells CulturedCOPDSmokingMiddle Agedmedicine.anatomical_structureBenzamidesCorticosteroidViral exacerbationDrug Therapy CombinationFemalePulmones - Enfermedadesmedicine.drugSignal TransductionAgonistPulmonary and Respiratory Medicinemedicine.medical_specialtymedicine.drug_classCorticosteroid resistanceBronchiInternal medicinemedicineCOPDHumansInterleukin 8DexamethasoneRoflumilastAgedLungbusiness.industryResearchInterleukin-8Epithelial CellsAparato respiratoriomedicine.diseaserespiratory tract diseasesToll-Like Receptor 3EndocrinologyPoly I-CCase-Control StudiesTLR3businessRespiratory Research
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Activation of the human immune system via toll-like receptors by the oncolytic parvovirus H-1.

2012

This study aimed to investigate the function of toll-like receptors (TLRs) during oncolytic parvovirus H-1 (H-1PV)-induced human immune responses. First, the role of TLRs in the activation of the NFκB transcription factor was characterized; second, the immunologic effects of H-1PV-induced tumor cell lysates (TCL) on human antitumor immune responses were evaluated. A human ex vivo model was used to study immune responses with dendritic cells (DCs). Human embryonic kidney cells (HEK293) transfected to stably express TLRs were used as potential human DC equivalents to further investigate the role of specific TLRs during immune activation. TLR3 and TLR9 were activated by H-1PV infection, which …

Cytotoxicity ImmunologicH-1 parvovirusCancer ResearchCytoplasmParvovirus H-1chemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayBiologyKidneyProinflammatory cytokineParvoviridae InfectionsImmune systemTumor Cells CulturedHumansMelanomaCells CulturedCell NucleusOncolytic VirotherapyTumor Necrosis Factor-alphaToll-Like ReceptorsNF-kappa BDendritic CellsAcquired immune systemFlow CytometryCell biologyOncolytic virusOncolytic VirusesOncologyImmune SystemImmunologyTLR3CytokinesTumor necrosis factor alphaSignal transductionSignal TransductionInternational journal of cancer
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Mast cells as rapid innate sensors of cytomegalovirus by TLR3/TRIF signaling-dependent and -independent mechanisms

2014

The succinct metaphor, ‘the immune system's loaded gun', has been used to describe the role of mast cells (MCs) due to their storage of a wide range of potent pro-inflammatory and antimicrobial mediators in secretory granules that can be released almost instantly on demand to fight invaders. Located at host–environment boundaries and equipped with an arsenal of pattern recognition receptors, MCs are destined to be rapid innate sensors of pathogens penetrating endothelial and epithelial surfaces. Although the importance of MCs in antimicrobial and antiparasitic defense has long been appreciated, their role in raising the alarm against viral infections has been noted only recently. Work on cy…

MaleChemokineImmunologyCytomegalovirusBiologyCD8-Positive T-LymphocytesCCL5MiceImmune systemImmunology and AllergyCytotoxic T cellAnimalsMast CellsMice KnockoutIntegrasesMacrophagesDegranulationPattern recognition receptorhumanitiesToll-Like Receptor 3Killer Cells NaturalMice Inbred C57BLAdaptor Proteins Vesicular TransportInfectious DiseasesTRIFImmunologyTLR3Cytomegalovirus Infectionsbiology.proteinFemaleResearch Article
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Cancer cell–autonomous contribution of type I interferon signaling to the efficacy of chemotherapy

2014

International audience; The immune system is routinely confronted with cell death resulting from the physiological turnover of renewable tissues, as well as from pathological insults of several types. We hypothesize the existence of a mechanism that allows the immune system to discriminate between physiological and pathological instances of cell death, but the factors that determine whether cellular demise is perceived as a neutral, tolerogenic or immunogenic event remain unclear 1. Infectious insults are accompanied by so-called microbe-associated molecular patterns (MAMPs), i.e., viral or bacterial products that activate immune cells through a panel of pattern-recognition receptors (PRRs)…

Myxovirus Resistance ProteinsMessengerReceptor Interferon alpha-betaInbred C57BLchemotherapyInterferon alpha-betaMiceInterferonReceptorsAnthracyclinesNeoplasm MetastasisRIG-IPattern recognition receptorAdaptor ProteinsGeneral MedicineNeoadjuvant Therapy3. Good healthGene Expression Regulation NeoplasticTreatment OutcomeReceptors Pattern RecognitionInterferon Type I[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleImmunocompetencemedicine.drugReceptorSignal TransductionBreast Neoplasms[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPattern RecognitionSettore BIO/09General Biochemistry Genetics and Molecular BiologyParacrine signallingImmune systemmedicineCXCL10AnimalsHumanscancerRNA MessengerAutocrine signallingNeoplastic[SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/ImmunotherapyToll-Like Receptor 3Mice Inbred C57BLVesicular TransportChemokine CXCL10Adaptor Proteins Vesicular TransportGene Expression RegulationDoxorubicinImmunologyTLR3RNAAdaptor Proteins Vesicular Transport; Animals; Anthracyclines; Breast Neoplasms; Chemokine CXCL10; Doxorubicin; Female; Gene Expression Regulation Neoplastic; Humans; Immunocompetence; Interferon Type I; Mice Inbred C57BL; Myxovirus Resistance Proteins; Neoadjuvant Therapy; Neoplasm Metastasis; RNA; RNA Messenger; Receptor Interferon alpha-beta; Receptors Pattern Recognition; Toll-Like Receptor 3; Treatment Outcome; Signal Transduction
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