Search results for "TLR"

showing 10 items of 207 documents

Triggering of Toll-like Receptors in Old Individuals. Relevance for Vaccination

2019

Aging is characterized by a general decline in a range of physiological functions, with a consequent increase in the risk of developing a variety of chronic diseases and geriatric syndromes. Additionally, increasing age is accompanied by a progressive decline in both innate and acquired immune system, referred to as immunosenescence. This impaired ability to mount an efficient immune response after exposure to microorganisms or vaccines represents a major challenge in acquiring protection against pathogens in aging. Therefore, there is still a great need for vaccines that are tailored to optimally stimulate the aged immune system, thus promoting more successful aging. Various strategies ca…

0301 basic medicineAgingCellular immunityImmunosenescencemedicine.medical_treatmentDendritic cells03 medical and health sciences0302 clinical medicineImmune systemAdjuvants ImmunologicImmunityTLRDrug DiscoverymedicineHumansAgedAged 80 and overPharmacologyImmunity CellularInnate immune systembusiness.industryToll-Like ReceptorsVaccinationImmunosenescenceAcquired immune systemVaccination030104 developmental biologyImmunologyCytokinesbusinessAdjuvant030215 immunologyCurrent Pharmaceutical Design
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Double methylation of tRNA-U54 to 2′-O-methylthymidine (Tm) synergistically decreases immune response by Toll-like receptor 7

2018

Abstract Sensing of nucleic acids for molecular discrimination between self and non-self is a challenging task for the innate immune system. RNA acts as a potent stimulus for pattern recognition receptors including in particular human Toll-like receptor 7 (TLR7). Certain RNA modifications limit potentially harmful self-recognition of endogenous RNA. Previous studies had identified the 2′-O-methylation of guanosine 18 (Gm18) within tRNAs as an antagonist of TLR7 leading to an impaired immune response. However, human tRNALys3 was non-stimulatory despite lacking Gm18. To identify the underlying molecular principle, interferon responses of human peripheral blood mononuclear cells to differentia…

0301 basic medicineBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMethylation03 medical and health sciencesRNA TransferInterferonNucleic Acids[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]RNA and RNA-protein complexesGeneticsmedicineHumansComputingMilieux_MISCELLANEOUSToll-like receptorInnate immune systemGuanosine030102 biochemistry & molecular biologyPattern recognition receptorRNA[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyTLR7Immunity InnateCell biology030104 developmental biologyToll-Like Receptor 7Transfer RNALeukocytes MononuclearNucleic acid[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]InterferonsHydrogenThymidinemedicine.drug
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The Involvement of Toll-like Receptor-2 in Arterial Thrombus Formation.

2018

There is emerging evidence for the participation of toll-like receptor-2 (TLR2) expressed on platelets and endothelial cells in the setting of arterial thrombosis. In isolated human platelets, TLR2/1 activation was demonstrated to induce platelet activation, secretion, aggregation, adhesion to collagen coatings and the formation of platelet-leukocyte conjugates, whereas murine platelets were less sensitive to TLR2/1 stimulation. Also, endothelial cells can be activated by stimulation with TLR2 agonists, resulting in increased expression of adhesion molecules, synthesis of inflammatory mediators and Weibel-Palade body exocytosis. Endothelial TLR2 signalling promotes atherosclerotic lesion de…

0301 basic medicineBlood Platelets030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineVon Willebrand factormedicineAnimalsHumansPlateletPlatelet activationInflammationToll-like receptorbiologyCell adhesion moleculeChemistryEndothelial CellsCarotid Artery ThrombosisThrombosisHematologyArteriesmedicine.diseasePlatelet ActivationThrombosisPlaque AtheroscleroticToll-Like Receptor 2TLR2030104 developmental biologyCancer researchbiology.proteinHamostaseologie
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Gut microbiota regulate hepatic von Willebrand factor synthesis and arterial thrombus formation via Toll-like receptor-2.

2016

The symbiotic gut microbiota play pivotal roles in host physiology and the development of cardiovascular diseases, but the microbiota-triggered pattern recognition signaling mechanisms that impact thrombosis are poorly defined. In this article, we show that germ-free (GF) and Toll-like receptor-2 (Tlr2)-deficient mice have reduced thrombus growth after carotid artery injury relative to conventionally raised controls. GF Tlr2-/- and wild-type (WT) mice were indistinguishable, but colonization with microbiota restored a significant difference in thrombus growth between the genotypes. We identify reduced plasma levels of von Willebrand factor (VWF) and reduced VWF synthesis, specifically in he…

0301 basic medicineBlood Plateletsmedicine.medical_specialtyEndotheliumPlatelet AggregationImmunologyBiologyBiochemistry03 medical and health sciencesMiceVon Willebrand factorhemic and lymphatic diseasesInternal medicinevon Willebrand FactormedicineAnimalsGerm-Free LifePlateletThrombusIntegrin bindingMice KnockoutToll-like receptorThrombosisCell BiologyHematologymedicine.diseaseToll-Like Receptor 2Gastrointestinal MicrobiomeTLR2030104 developmental biologymedicine.anatomical_structureEndocrinologyLivercardiovascular systembiology.proteinSignal transductioncirculatory and respiratory physiologySignal TransductionBlood
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Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

2019

Summary MyD88, an adaptor molecule downstream of innate pathways, plays a significant tumor-promoting role in sporadic intestinal carcinogenesis of the Apcmin/+ model, which carries a mutation in the Apc gene. Here, we show that deletion of MyD88 in intestinal mesenchymal cells (IMCs) significantly reduces tumorigenesis in this model. This phenotype is associated with decreased epithelial cell proliferation, altered inflammatory and tumorigenic immune cell infiltration, and modified gene expression similar to complete MyD88 knockout mice. Genetic deletion of TLR4, but not interleukin-1 receptor (IL-1R), in IMCs led to altered molecular profiles and reduction of intestinal tumors similar to …

0301 basic medicineCarcinogenesisBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciences0302 clinical medicinemedicinetumor microenvironmentAnimalsHumansReceptorinnate immunityTumor microenvironmentInnate immune systemMesenchymal stem cellCell biologyIntestinesToll-Like Receptor 4030104 developmental biologyMyeloid Differentiation Factor 88Knockout mouseTLR4Carcinogenesiscancer-associated fibroblasts030217 neurology & neurosurgerySignal Transduction
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CD14 is a key organizer of microglial responses to CNS infection and injury

2015

Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon β-mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced …

0301 basic medicineChemokineToll-like receptorInnate immune systembiologyMicrogliaCD14Proinflammatory cytokine03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologymedicine.anatomical_structureImmune systemNeurologyImmunologybiology.proteinTLR4medicineGlia
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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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Identification of an optimized 2′-O-methylated trinucleotide RNA motif inhibiting Toll-like receptors 7 and 8

2017

Bacterial RNA serves an important function as activator of the innate immune system. In humans bacterial RNA is sensed by the endosomal receptors TLR7 and TLR8. Differences in the posttranscriptional modification profile of prokaryotic when compared with eukaryotic RNA allow innate immune cells to discriminate between “host” and “foreign” RNA. Ribose 2′-O-methylation is of particular importance and has been reported to antagonize TLR7/8 activation. Yet, the exact sequence context in which 2′-O-methylation has to occur to mediate its inhibitory activity remains largely undefined. On the basis of a naturally occurring 2′-O-methylated RNA sequence, we performed a systematic permutation of the …

0301 basic medicineCytidineBiologyBioinformaticsMethylationInhibitory Concentration 5003 medical and health scienceschemistry.chemical_compound0302 clinical medicineRNA TransferReportRiboseHumansNucleotideNucleotide MotifsMolecular Biologychemistry.chemical_classificationInnate immune systemNucleotides2'-O-methylationRNATLR7TLR8Cell biologyRNA Bacterial030104 developmental biologyToll-Like Receptor 7chemistryToll-Like Receptor 8MutationLeukocytes MononuclearNucleic acidRNA030215 immunologyRNA
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DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

2018

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not…

0301 basic medicineGenome instabilityDNA damageLipoproteinsCellMitosisInflammationAtaxia Telangiectasia Mutated ProteinsBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicemedicineAnimalsHumansMacrophage Differentiation PathwayMitosisCell ProliferationInflammationGranulomaMacrophagesCell DifferentiationMycobacterium tuberculosisToll-Like Receptor 2Cell biologyMice Inbred C57BLTLR2030104 developmental biologymedicine.anatomical_structureImmunologymedicine.symptomCarcinogenesisDNA DamageCell
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Adipocytes as a Link Between Gut Microbiota-Derived Flagellin and Hepatocyte Fat Accumulation

2016

While the role of both elevated levels of circulating bacterial cell wall components and adipose tissue in hepatic fat accumulation has been recognized, it has not been considered that the bacterial components-recognizing adipose tissue receptors contribute to the hepatic fat content. In this study we found that the expression of adipose tissue bacterial flagellin (FLG)-recognizing Toll-like receptor (TLR) 5 associated with liver fat content (r = 0.699, p = 0.003) and insulin sensitivity (r = -0.529, p = 0.016) in humans (n = 23). No such associations were found for lipopolysaccharides (LPS)-recognizing TLR4. To study the underlying molecular mechanisms of these associations, human HepG2 he…

0301 basic medicineGlycerollcsh:MedicineAdipose tissueWhite adipose tissueflagellinBiochemistryImmune ReceptorsFatsEndocrinologyAnimal CellsAdipocytesMedicine and Health SciencesInsulinlcsh:ScienceToll-like ReceptorsConnective Tissue CellsMultidisciplinaryImmune System ProteinsbiologyLiver DiseasesFatty liverin kaltaiset reseptorit [toll]Lipidsadipose tissuePhysical sciencesChemistryMitochondrial respiratory chainAdipose TissueConnective Tissuebacterial componentsCellular TypesAnatomyinsuline sensitivityResearch ArticleSignal Transductionmedicine.medical_specialtyadipocytesImmunologyMonomers (Chemistry)Gastroenterology and Hepatologyta311103 medical and health sciencesInsulin resistanceInternal medicinemedicinePolymer chemistryDiabetic Endocrinologylcsh:Rta1183ta1182Biology and Life SciencesProteinsCell Biologyliver fatmedicine.diseasehepatic fatfat accumulationHormonesIRS1Fatty LiverInsulin receptor030104 developmental biologyEndocrinologyBiological TissueTLR5biology.proteinlcsh:QPLoS ONE
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