Search results for "Toll"

showing 10 items of 324 documents

Bioconjugation of Small Molecules to RNA Impedes Its Recognition by Toll-Like Receptor 7

2017

A fundamental mechanism of the innate immune system is the recognition, via extra- and intracellular pattern recognition receptors, of pathogen-associated molecular patterns. A prominent example is represented by foreign nucleic acids, triggering the activation of several signaling pathways. Among these, the endosomal toll-like receptor 7 (TLR7) is known to be activated by single stranded RNA (ssRNA), which can be specifically influenced through elements of sequence structure and posttranscriptional modifications. Furthermore, small molecules TLR7 agonists (smTLRa) are applied as boosting adjuvants in vaccination processes. In this context, covalent conjugations between adjuvant and vaccine…

0301 basic medicineMessenger RNAGene knockdownToll-like receptormRNAImmunologyPattern recognition receptorRNATLR7BiologyMolecular biologyCell biology03 medical and health sciencessmall molecules030104 developmental biologysiRNAclick chemistryNucleic acidImmunology and Allergytoll-like receptorimmunostimulationbioconjugateSingle-Stranded RNAOriginal ResearchFrontiers in Immunology
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Systemic Candidiasis and TLR2 Agonist Exposure Impact the Antifungal Response of Hematopoietic Stem and Progenitor Cells.

2018

We have previously demonstrated that Candida albicans induces differentiation of hematopoietic stem and progenitor cells (HSPCs) toward the myeloid lineage both in vitro and in vivo in a TLR2- and Dectin-1-dependent manner, giving rise to functional macrophages. In this work, we used an ex vivo model to investigate the functional consequences for macrophages derived from HSPCs in vivo-exposed to Pam3CSK4 (a TLR2 agonist) or C. albicans infection. Short in vivo treatment of mice with Pam3CSK4 results in a tolerized phenotype of ex vivo HSPC-derived macrophages, whereas an extended Pam3CSK4 treatment confers a trained phenotype. Early during candidiasis, HSPCs give rise to macrophages trained…

0301 basic medicineMicrobiology (medical)medicine.medical_treatmenthematopoietic stem and progenitor cellsImmunologylcsh:QR1-502Colony Count MicrobialBiologyKidneyMicrobiologylcsh:Microbiology03 medical and health sciencesLipopeptidesMiceCandida albicansmedicineTLR2host-pathogen interactionsMacrophageAnimalsProgenitor cellCandida albicansinnate immunityInnate immune systemMacrophagesCandidiasisCell Differentiationbiology.organism_classificationmedicine.diseaseHematopoietic Stem CellsToll-Like Receptor 2Haematopoiesis030104 developmental biologyInfectious DiseasesCytokineImmunologySystemic candidiasisEx vivoSpleenFrontiers in cellular and infection microbiology
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Notch and TLR signaling coordinate monocyte cell fate and inflammation

2020

AbstractConventional Ly6Chi monocytes have developmental plasticity for a spectrum of differentiated phagocytes. Here we show, using conditional deletion strategies in a mouse model of Toll-like receptor (TLR) 7-induced inflammation, that the spectrum of developmental cell fates of Ly6Chi monocytes, and the resultant inflammation, is coordinately regulated by TLR and Notch signaling. Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions, while impairment in either signaling axis impairs Ly6Clo monocyte development. At the same time, TLR7 stimulation in the absence of …

0301 basic medicineMouseQH301-705.5ScienceNotch signaling pathwayInflammationSpleenBiologyCell fate determinationSystemic inflammationGeneral Biochemistry Genetics and Molecular BiologyMonocytesimmunology03 medical and health sciencesMice0302 clinical medicineImmunology and InflammationmedicineAnimalsReceptor Notch2Biology (General)Receptormousemacrophage differentiationInflammationMembrane GlycoproteinsGeneral Immunology and MicrobiologyGeneral NeuroscienceMonocyteQRCell DifferentiationTLR signalingGeneral MedicineTLR7notch signalingCell biology030104 developmental biologymedicine.anatomical_structureToll-Like Receptor 7inflammationmonocytes and macrophagesMedicinemedicine.symptom030215 immunologySignal TransductionResearch Article
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The murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated trans…

2017

The type I interferon (IFN) response is imperative for the establishment of the early antiviral immune response. Here we report the identification of the first type I IFN antagonist encoded by murine cytomegalovirus (MCMV) that shuts down signaling following pattern recognition receptor (PRR) sensing. Screening of an MCMV open reading frame (ORF) library identified M35 as a novel and strong negative modulator of IFNβ promoter induction following activation of both RNA and DNA cytoplasmic PRR. Additionally, M35 inhibits the proinflammatory cytokine response downstream of Toll-like receptors (TLR). Using a series of luciferase-based reporters with specific transcription factor binding sites, …

0301 basic medicineMuromegalovirusPhysiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMiceWhite Blood Cells0302 clinical medicineCell SignalingTranscription (biology)InterferonAnimal CellsImmune PhysiologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Enzyme-Linked ImmunoassaysReceptorConnective Tissue CellsbiologyToll-Like ReceptorsPattern recognition receptorNF-kappa BImmune Receptor SignalingEnzymesThe murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated transcription.Connective TissueReceptors Pattern RecognitionCytomegalovirus InfectionsInterferon Type ISignal transductionCellular TypesAnatomyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.OxidoreductasesLuciferasemedicine.drugProtein BindingSignal TransductionResearch ArticleViral proteinQH301-705.5Immune CellsImmunologyResearch and Analysis MethodsTransfectionMicrobiology03 medical and health sciencesViral ProteinsMuromegalovirusVirologyGeneticsmedicineAnimalsImmunoassaysMolecular Biology TechniquesMolecular BiologyBlood CellsMacrophagesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Biology and Life SciencesProteinsNF-κBInterferon-betaCell BiologyRC581-607Fibroblastsbiology.organism_classificationMolecular biology030104 developmental biologyBiological TissuechemistryEnzymologyImmunologic TechniquesParasitologyInterferonsImmunologic diseases. AllergySpleen030215 immunology
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Binge-like ethanol treatment in adolescence impairs autophagy and hinders synaptic maturation: Role of TLR4.

2018

Abstract Adolescence is a developmental period of brain maturation in which remodeling and changes in synaptic plasticity and neural connectivity take place in some brain regions. A different mechanism participates in adolescent brain maturation, including autophagy processes that play a role in synaptic development and plasticity. Alcohol is a neurotoxic compound whose abuse in adolescence causes TLR4 response activation by triggering neuroinflammation, neural damage and behavioral alterations. However, the potential participation of autophagy in long-term neurochemical and cognitive dysfunctions induced by binge ethanol drinking in adolescence is uncertain. We therefore evaluated whether …

0301 basic medicineNeurogenesisImmune receptorBiologyBinge Drinking03 medical and health sciencesMice0302 clinical medicineNeurochemicalAutophagyAnimalsTLR4PI3K/AKT/mTOR pathwayNeuroinflammationMice KnockoutBinge ethanol treatmentEthanolGeneral NeuroscienceAutophagyAge FactorsAdolescenceMice Inbred C57BLToll-Like Receptor 4030104 developmental biologyStructural synaptic plasticitySynaptic plasticitySynapsesExcitatory postsynaptic potentialTLR4FemaleNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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Nano-Enhanced Cancer Immunotherapy: Immunology Encounters Nanotechnology

2020

Cancer immunotherapy utilizes the immune system to fight cancer and has already moved from the laboratory to clinical application. However, and despite excellent therapeutic outcomes in some hematological and solid cancers, the regular clinical use of cancer immunotherapies reveals major limitations. These include the lack of effective immune therapy options for some cancer types, unresponsiveness to treatment by many patients, evolving therapy resistance, the inaccessible and immunosuppressive nature of the tumor microenvironment (TME), and the risk of potentially life-threatening immune toxicities. Given the potential of nanotechnology to deliver, enhance, and fine-tune cancer immunothera…

0301 basic medicinePD-L1medicine.medical_treatmentimmune checkpoint inhibitorNanotechnologyReviewmacrophage03 medical and health sciencesMice0302 clinical medicineImmune systemDrug Delivery SystemsCancer immunotherapyPD-L1NeoplasmsPD-1MedicineAnimalsHumansNanotechnologytumor microenvironmentTreatment resistanceAdverse effecttoll like receptor (TLR)lcsh:QH301-705.5Tumor microenvironmentbiologybusiness.industryCancerGeneral Medicinemedicine.diseaseCombined Modality TherapyImmune therapy030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesissiRNAbiology.proteinCAR T cell therapymyeloid derived suppressor cells (MDSC)Immunotherapybusinessbi-specific antibody therapyCells
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Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

2017

Recent advances in the field of innate immunity have revealed a complex role of innate immune signaling pathways in both tissue homeostasis and disease. Among them, the Toll-like receptor 4 (TLR-4) pathways has been linked to various pathophysiological conditions, such as cardiovascular diseases (CVDs). This has been interrogated by developing multiple laboratory tools that have shown in animal models and clinical conditions, the involvement of the TLR-4 signaling pathway in the pathophysiology of different CVDs, such as atherosclerosis, ischemic heart disease, heart failure, ischemia-reperfusion injury and aorta aneurysm. Among these, aorta aneurysm, a very complex pathological condition w…

0301 basic medicinePathologymedicine.medical_specialtyAgingDisease030204 cardiovascular system & hematologyBioinformatics03 medical and health sciences0302 clinical medicineAneurysmAorta; Aorta aneurysms; TLR-4 signaling pathway; Treatments; Aging; Animals; Aorta; Cardiovascular Diseases; Homeostasis; Humans; Toll-Like Receptor 4; Signal TransductionAorta aneurysmsmedicine.arterymedicineSettore MED/05 - Patologia ClinicaAnimalsHomeostasisHumansMolecular BiologyTissue homeostasisAortaToll-like receptorAortaAorta; Aorta aneurysms; TLR-4 signaling pathway; TreatmentsInnate immune systembusiness.industryTreatmentsTLR-4 signaling pathwaySettore MED/23 - Chirurgia Cardiacamedicine.diseaseToll-Like Receptor 4030104 developmental biologyCardiovascular DiseasesHeart failurecardiovascular systemAorta aneurysmSignal transductionCardiology and Cardiovascular MedicinebusinessSignal Transduction
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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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Nutritional Wheat Amylase-Trypsin Inhibitors Promote Intestinal Inflammation via Activation of Myeloid Cells.

2016

Background & Aims Wheat amylase-trypsin inhibitors (ATIs) are nutritional activators of innate immunity, via activation of the toll-like receptor 4 (TLR4) on myeloid cells. We aimed to characterize the biologic activity of ATIs in various foods and their effect on intestinal inflammation. Methods We selected 38 different gluten-containing and gluten-free products, either unprocessed (such as wheat, rye, barley, quinoa, amaranth, soya, lentils, and rice) or processed (such as pizza, pasta, bread, and biscuits). ATIs were extracted and their biological activities determined in TLR4-responsive mouse and human cell lines. Effects of oral ATIs on intestinal inflammation were determined in health…

0301 basic medicinePharmacologyAdaptive Immunitychemistry.chemical_compoundMice0302 clinical medicineMesenteric lymph nodesMesenteryMyeloid CellsTriticumPlant ProteinsToll-like receptorDextran SulfateGastroenterologyfood and beveragesColitisIntestinesmedicine.anatomical_structureAmylases030211 gastroenterology & hepatologymedicine.symptomTrypsin InhibitorsInterferon InducersGlutensColonDuodenumInflammationIleumBiologyCell Line03 medical and health sciencesDiet Gluten-FreeIleummedicineAnimalsHumansColitisInflammationInnate immune systemHepatologymedicine.diseaseImmunity InnateMice Inbred C57BLToll-Like Receptor 4Celiac Disease030104 developmental biologyPoly I-CchemistryPolyinosinic:polycytidylic acidImmunologyLymph NodesWheat allergyGastroenterology
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Mechanical ventilation alters the development of staphylococcus aureus pneumonia in rabbit

2016

Ventilator-associated pneumonia (VAP) is common during mechanical ventilation (MV). Beside obvious deleterious effects on muco-ciliary clearance, MV could adversely shift the host immune response towards a pro-inflammatory pattern through toll-like receptor (TLRs) up-regulation. We tested this hypothesis in a rabbit model of Staphylococcus aureus VAP. Pneumonia was caused by airway challenge with S. aureus, in either spontaneously breathing (SB) or MV rabbits (n = 13 and 17, respectively). Pneumonia assessment regarding pulmonary and systemic bacterial burden, as well as inflammatory response was done 8 and 24 hours after S. aureus challenge. In addition, ex vivo stimulations of whole blood…

0301 basic medicinePulmonologyPhysiologyStaphylococcusmedicine.medical_treatment[SDV]Life Sciences [q-bio]lcsh:MedicinePharmacologyPathology and Laboratory Medicinemedicine.disease_causeStaphylococcal/immunology/pathologyImmune ReceptorsBiochemistry0302 clinical medicineImmune PhysiologyPneumonia StaphylococcalMedicine and Health SciencesMedicineStaphylococcus Aureuslcsh:ScienceImmune ResponseToll-like ReceptorsMammalsddc:616Innate Immune SystemImmune System ProteinsMultidisciplinaryddc:617RespirationPneumonia Ventilator-AssociatedInterleukinAnimal ModelsHematologyBacterial PathogensBody Fluids3. Good healthBloodmedicine.anatomical_structureMedical MicrobiologyStaphylococcus aureusVertebratesArtificialCytokinesRabbitsPathogensAnatomymedicine.symptomStaphylococcus aureus/immunologyResearch ArticleSignal TransductionToll-Like Receptor 2/immunologyImmunologyInflammationLung injuryResearch and Analysis MethodsMicrobiology03 medical and health sciencesModel OrganismsSigns and SymptomsDiagnostic MedicineAnimalsMicrobial PathogensInflammationMechanical ventilationInterleukin-8/immunologyLung[ SDV ] Life Sciences [q-bio]BacteriaTumor Necrosis Factor-alphabusiness.industrylcsh:RInterleukin-8OrganismsBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyPneumoniaMolecular Developmentmedicine.diseaseTumor Necrosis Factor-alpha/immunologyRespiration ArtificialToll-Like Receptor 2Pneumonia030104 developmental biologyVentilator-Associated/immunology/microbiology/pathologyImmune SystemAmniotesImmunologylcsh:QbusinessSpleenEx vivoDevelopmental Biology
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