Search results for "toll"

showing 10 items of 324 documents

Autoimmune skin inflammation is dependent on plasmacytoid dendritic cell activation by nucleic acids via TLR7 and TLR9

2010

Lupus-prone mice develop a chronic inflammatory response to cutaneous injury that depends on the production of type I interferon, TLR7, and TLR9.

MaleMice 129 StrainImmunologyGene ExpressionInflammationchemical and pharmacologic phenomenaMice Inbred StrainsReceptor Interferon alpha-betaBiologySkin DiseasesArticleProinflammatory cytokinePathogenesisTLR9MiceAutoimmune skin inflammationimmune system diseasesNucleic AcidsmedicineImmunology and AllergyAnimalsLupus Erythematosus SystemicReceptorskin and connective tissue diseasesTLR7SkinAutoimmune skin inflammation; TLR7; TLR9; plasmacytoid dendritic cells.Mice KnockoutPlasmacytoid dendritic cell activationLupus erythematosusReverse Transcriptase Polymerase Chain ReactionTLR9virus diseaseshemic and immune systemsTLR7DNADendritic Cellsmedicine.diseaseFlow CytometryMice Inbred C57BLplasmacytoid dendritic cells.Toll-Like Receptor 7Toll-Like Receptor 9ImmunologyMyeloid Differentiation Factor 88CytokinesFemalemedicine.symptomThe Journal of Experimental Medicine
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MyD88 is dispensable for resistance toParacoccidioides brasiliensisin a murine model of blood-borne disseminated infection

2008

We have studied the role of MyD88, an adaptor protein of Toll-like receptors (TLRs), in murine defenses against Paracoccidioides brasiliensis in a model of blood-borne disseminated infection. Wild-type (WT) and MyD88-deficient mice infected intravenously with P. brasiliensis yeast cells showed an equivalent fungal burden, as well as similar levels of proinflammatory IL-1beta, IL-6, IL-12p70, tumor necrosis factor (TNF)-alpha and MIP-2, T-helper type 1 (Th1) (IFN-gamma) and Th2 cytokines (IL-4) in tissue homogenates. In vitro production of TNF-alpha, IFN-gamma and IL-12p70, by antigen-stimulated splenocytes from infected animals, was also similar in both types of mice; this production of Th1…

MaleMicrobiology (medical)medicine.medical_treatmentImmunologyNerve Tissue ProteinsMicrobiologyParacoccidioidesMicrobiologyProinflammatory cytokineMicePeritoneal cavitymedicineAnimalsHumansImmunology and AllergyLectins C-TypeMice KnockoutParacoccidioides brasiliensisbiologyMembrane ProteinsParacoccidioidesGeneral MedicineTh1 Cellsbiology.organism_classificationToll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4Disease Models AnimalTLR2Infectious Diseasesmedicine.anatomical_structureCytokineMyeloid Differentiation Factor 88Macrophages PeritonealTLR4CytokinesTumor necrosis factor alphaParacoccidioidomycosisFungemiaFEMS Immunology & Medical Microbiology
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Dectin-1 Stimulation of Hematopoietic Stem and Progenitor Cells Occurs In Vivo and Promotes Differentiation Toward Trained Macrophages via an Indirec…

2020

Invasive candidiasis is an increasingly frequent cause of serious and often fatal infections. Understanding host defense is essential to design novel therapeutic strategies to boost immune protection against Candida albicans. In this article, we delve into two new concepts that have arisen over the last years: (i) the delivery of myelopoiesis-inducing signals by microbial components directly sensed by hematopoietic stem and progenitor cells (HSPCs) and (ii) the concept of “trained innate immunity” that may also apply to HSPCs. We demonstrate that dectin-1 ligation in vivo activates HSPCs and induces their differentiation to trained macrophages by a cell-autonomous indirect mechanism. This p…

MaleMyeloidbeta-Glucanshematopoietic stem and progenitor cellstlr2BiologyMicrobiologyHost-Microbe Biology03 medical and health sciencesMicetrained immunity0302 clinical medicineImmune systemVirologymedicineAnimalsLectins C-TypeProgenitor cell030304 developmental biologyMice Knockout0303 health sciencesInnate immune systemStem CellsCandidiasisCell DifferentiationHematopoietic Stem CellsImmunity InnateToll-Like Receptor 2QR1-502Cell biologymacrophagesTransplantationMice Inbred C57BLTLR2Haematopoiesismedicine.anatomical_structureMyeloid Differentiation Factor 88Femalecandida albicansBone marrowdectin-1030215 immunologyResearch ArticleSignal TransductionmBio
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Toll-like receptor 4 defective mice carrying point or null mutations do not show increased susceptibility toCandida albicansin a model of hematogenou…

2006

We have studied the role of TLR4 in murine defenses against Candida albicans in two TLR4-defective mouse strains: C3H/HeJ mice which have defective TLR4 signaling, and TLR4-/- knockout mice. Both TLR4-defective mice strains experimentally infected with virulent C. albicans cells showed no significant difference in survival as compared with their respective controls. Recruitment of neutrophils to the peritoneal cavity of i.p. infected mice was not affected in TLR4-/-animals, but significantly enhanced in C3H/HeJ mice, compared with their control mice. In vitro production of TNF-alpha by macrophages from both types of TLR4-defective mice, in response to yeasts and hyphae of C. albicans, was n…

MaleNeutrophilsBiologyMicrobiologyInterferon-gammaMicePeritoneal cavityCandida albicansSplenocytemedicineAnimalsPoint MutationGenetic Predisposition to DiseaseCandida albicansMice KnockoutMice Inbred C3HToll-like receptorTumor Necrosis Factor-alphaCandidiasisGeneral MedicineTh1 CellsFlow Cytometrybiology.organism_classificationInterleukin-12Corpus albicansMice Inbred C57BLToll-Like Receptor 4Infectious Diseasesmedicine.anatomical_structureKnockout mouseMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Tumor necrosis factor alphaMedical Mycology
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Susceptibility to infection with Borrelia afzelii and TLR2 polymorphism in a wild reservoir host

2019

AbstractThe study of polymorphic immune genes in host populations is critical for understanding genetic variation in susceptibility to pathogens. Controlled infection experiments are necessary to separate variation in the probability of exposure from genetic variation in susceptibility to infection, but such experiments are rare for wild vertebrate reservoir hosts and their zoonotic pathogens. The bank vole (Myodes glareolus) is an important reservoir host of Borrelia afzelii, a tick-borne spirochete that causes Lyme disease. Bank vole populations are polymorphic for Toll-like receptor 2 (TLR2), an innate immune receptor that recognizes bacterial lipoproteins. To test whether the TLR2 polym…

MaleNymph0301 basic medicinemetsämyyrälcsh:MedicineTickBorrelia afzeliimedicine.disease_causeinfektiotgenotyyppiArticle03 medical and health sciencesTicks0302 clinical medicineLyme diseaseBorrelia burgdorferi GroupPolymorphism (computer science)GenotypeGenetic variationparasitic diseasesisäntäeläimetImmunogeneticsmedicineAnimalsimmuniteettiGenetic Predisposition to Diseaselcsh:ScienceDisease ReservoirsGeneticsLyme DiseasePolymorphism GeneticMultidisciplinaryInnate immune systembiologyArvicolinaelcsh:REcological geneticsmedicine.diseasebiology.organism_classificationbacterial infections and mycosesToll-Like Receptor 2Borrelia-bakteeritBank vole030104 developmental biology[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyFemalelcsh:Q030217 neurology & neurosurgeryClethrionomys
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Polymorphisms of an innate immune gene, toll-like receptor 4, and aggressive prostate cancer risk: a systematic review and meta-analysis.

2014

Background: Toll-like receptor 4 (TLR4) is one of the best known TLR members expressed on the surface of several leukocytes and tissue cells and has a key function in detecting pathogen and danger-associated molecular patterns. The role of TLR4 in the pathophysiology of several age-related diseases is also well recognized, such as prostate cancer (PCa). TLR4 polymorphisms have been related to PCa risk, but the relationship between TLR4 genotypes and aggressive PCa risk has not been evaluated by any systematic reviews. Methods: We performed a systematic review and meta-analysis of candidate-gene and genome-wide association studies analyzing this relationship and included only white populatio…

MaleProstate cancer polymorphisms of TLR4 aggressive prostate cancer risk meta-analysisSystematic Reviewslcsh:MedicineGenome-wide association studySingle-nucleotide polymorphismBiologyResearch and Analysis MethodsBioinformaticsPolymorphism Single NucleotideProstate cancerGenotypeGeneticsCancer GeneticsmedicineHumansSettore MED/05 - Patologia ClinicaGenetic Predisposition to DiseaseStatistical Methodslcsh:ScienceGenotypingGenetic associationEvolutionary BiologyMultidisciplinarylcsh:RProstatic NeoplasmsBiology and Life SciencesResearch Assessmentmedicine.diseaseImmunity InnateToll-Like Receptor 4Systematic reviewMeta-analysisPhysical SciencesGenetic Polymorphismlcsh:QPopulation GeneticsMathematicsStatistics (Mathematics)Genome-Wide Association StudyResearch ArticleMeta-AnalysisPLoS ONE
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Interruption of Macrophage-Derived IL-27(p28) Production by IL-10 during Sepsis Requires STAT3 but Not SOCS3

2014

Abstract Severe sepsis and septic shock are leading causes of morbidity and mortality worldwide. Infection-associated inflammation promotes the development and progression of adverse outcomes in sepsis. The effects of heterodimeric IL-27 (p28/EBI3) have been implicated in the natural course of sepsis, whereas the molecular mechanisms underlying the regulation of gene expression and release of IL-27 in sepsis are poorly understood. We studied the events regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal ligation and puncture. Neutralizing Abs to IL-27(p28) improved survival rates, restricted cytokine release, and reduced bacterial burden in C57BL/…

MaleSTAT3 Transcription Factormedicine.medical_treatmentImmunologySuppressor of Cytokine Signaling ProteinsInflammationSpleenBiologyArticleSepsisMiceSepsismedicineAnimalsHumansImmunology and AllergyReceptors CytokineAntibodies BlockingCecumCells CulturedMice KnockoutSeptic shockInterleukinsMacrophagesReceptors Interleukinmedicine.diseaseBacterial LoadInterleukin-10Mice Inbred C57BLToll-Like Receptor 4Adaptor Proteins Vesicular TransportDisease Models AnimalOxidative StressInterleukin 10Cytokinemedicine.anatomical_structureIntegrin alpha MSuppressor of Cytokine Signaling 3 ProteinMyeloid Differentiation Factor 88ImmunologyTLR4biology.proteinmedicine.symptomJournal of Immunology
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TLR4 response mediates ethanol-induced neurodevelopment alterations in a model of fetal alcohol spectrum disorders

2017

Background Inflammation during brain development participates in the pathogenesis of early brain injury and cognitive dysfunctions. Prenatal ethanol exposure affects the developing brain and causes neural impairment, cognitive and behavioral effects, collectively known as fetal alcohol spectrum disorders (FASD). Our previous studies demonstrate that ethanol activates the innate immune response and TLR4 receptor and causes neuroinflammation, brain damage, and cognitive defects in the developmental brain stage of adolescents. We hypothesize that by activating the TLR4 response, maternal alcohol consumption during pregnancy triggers the release of cytokines and chemokines in both the maternal …

MaleSerum0301 basic medicineChemokineDevelopmental Disabilitiesmedicine.medical_treatmentlcsh:RC346-429MiceMyelin0302 clinical medicineNeuroinflammationPregnancyTLR4Maternal BehaviorFetal alcohol spectrum disordersMice KnockoutMicrogliabiologyGeneral NeuroscienceAge FactorsBrainCerebral cortexBehavior impairmentsmedicine.anatomical_structureCytokineNeurologyPrenatal Exposure Delayed EffectsCytokinesFemalemedicine.symptomMyelin ProteinsAmniotic fluidmedicine.medical_specialtyOffspringImmunologyNerve Tissue ProteinsBrain damage03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineAvoidance LearningmedicineAnimalsMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationEthanolbusiness.industryResearchBody WeightCentral Nervous System DepressantsMice Inbred C57BLToll-Like Receptor 4Disease Models AnimalMicroscopy Electron030104 developmental biologyEndocrinologyAnimals NewbornPrenatal ethanol exposureImmunologybiology.proteinTLR4business030217 neurology & neurosurgeryJournal of Neuroinflammation
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RNA recognition by human TLR8 can lead to autoimmune inflammation

2013

High expression level of human TLR8 in mice results in spontaneous, multiorgan inflammation attributable in part to increased DC activation.

MaleT cellT-LymphocytesImmunologyArthritisInflammationMice TransgenicAutoimmunityTRL8AUTOIMMUNE INFLAMMATIONBiologymedicine.disease_causeArticleAutoimmunityProinflammatory cytokineMiceTRL8; AUTOIMMUNE INFLAMMATIONhemic and lymphatic diseasesmedicineImmunology and AllergyAnimalsHumansTransgenesChildRandomized Controlled Trials as TopicInflammationGene Expression ProfilingTLR7TLR8medicine.diseaseArthritis Experimentaldigestive system diseasesArthritis JuvenileMice Inbred C57BLmedicine.anatomical_structureToll-Like Receptor 7Toll-Like Receptor 8ImmunologyRNAFemaleCollagenSignal transductionmedicine.symptomSignal TransductionThe Journal of Experimental Medicine
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Partial Sleep Restriction Activates Immune Response-Related Gene Expression Pathways: Experimental and Epidemiological Studies in Humans

2013

Epidemiological studies have shown that short or insufficient sleep is associated with increased risk for metabolic diseases and mortality. To elucidate mechanisms behind this connection, we aimed to identify genes and pathways affected by experimentally induced, partial sleep restriction and to verify their connection to insufficient sleep at population level. The experimental design simulated sleep restriction during a working week: sleep of healthy men (N = 9) was restricted to 4 h/night for five nights. The control subjects (N = 4) spent 8 h/night in bed. Leukocyte RNA expression was analyzed at baseline, after sleep restriction, and after recovery using whole genome microarrays complem…

MaleTBX21NF-KAPPA-Blcsh:MedicineNK cellsBioinformaticskokeellinen tutkimusReceptors G-Protein-Coupled0302 clinical medicineCARDIOMETABOLIC RISKLeukocytesta319geeniekspressiolcsh:Scienceta515Sleep restrictionRegulation of gene expression0303 health sciencesMultidisciplinaryNATURAL-KILLERNF-kappa Bta3142Sleep in non-human animalsC-REACTIVE PROTEIN3. Good healthMACROPHAGE APOPTOSISINSUFFICIENT SLEEPSTAT1 Transcription FactorCARDIOVASCULAR-DISEASEimmuunivasteProteoglycansmedicine.symptomResearch ArticleAdulteducationENDOPLASMIC-RETICULUMMETABOLIC CONSEQUENCESSyntaxin 16Biologyepidemiologinen tutkimusuni (lepotila)03 medical and health sciencesImmune systemmedicineHumans030304 developmental biologyTOLL-LIKE RECEPTORSB cellsuniMicroarray analysis techniquesGene Expression Profilingsytokiinitlcsh:RMicroarray AnalysisGene expression profilingSleep deprivationGene Expression RegulationImmunologyRNASleep Deprivationlcsh:Q3111 BiomedicineT-Box Domain ProteinsReceptors Transforming Growth Factor beta030217 neurology & neurosurgery
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