Search results for "Toll"

showing 10 items of 324 documents

Cigarette smoke alters IL-33 expression and release in airway epithelial cells

2014

AbstractAirway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored.Mini-BALs, but not sera, from smokers show red…

Bronchial epithelial cellLipopolysaccharidesBlotting WesternBronchiInflammationRespiratory MucosaBiologyReal-Time Polymerase Chain ReactionBronchoalveolar LavageImmunoenzyme TechniquesBronchial epithelial cell; COPD; Cigarette smoke; IL-33; InflammationSmokeacute lung injury cigarette smokeinterleukin 33medicineCOPDHumansRNA MessengerReceptorMolecular BiologyCells CulturedCell ProliferationInflammationToll-like receptorInnate immune systemReverse Transcriptase Polymerase Chain ReactionInterleukinsCigarette smokeFlow CytometryInterleukin-33Immunity Innaterespiratory tract diseasesCell biologyToll-Like Receptor 4Interleukin 33ImmunologyIL-33TLR4Molecular MedicineRespiratory epitheliummedicine.symptomIntracellularBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Glycoprotein 96-activated dendritic cells induce a CD8-biased T cell response.

2005

Heat shock proteins (Hsps) are able to induce protective immune responses against pathogens and tumors after injection into immunocompetent hosts. The activation of components of the adaptive immune system, including cytotoxic T lymphocytes specific for pathogen- or tumor-derived peptides, is crucial for the establishment of immuno- protection. Hsps acquire these peptides during intracellular protein degradation and when released during necrotic cell death, facilitate their uptake and Minor Histocompatibility Complex (MHC)-restricted representation by professional antigen-presenting cells (APCs). In addition, the interaction of Hsps with APCs, including the Endoplasmatic Reticulum (ER)-resi…

CD4-Positive T-LymphocytesLipopolysaccharidesAntigen-Presenting CellsBone Marrow CellsMice TransgenicReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexLymphocyte ActivationBiochemistryMiceImmune systemHeat shock proteinCytotoxic T cellAnimalsHumansAntigen-presenting cellCells CulturedMembrane GlycoproteinsToll-Like ReceptorsCell DifferentiationCell BiologyDendritic cellDendritic CellsOriginal ArticlesAcquired immune systemLymphocyte SubsetsCell biologyMice Inbred C57BLToll-Like Receptor 4biology.proteinInflammation MediatorsCD8Signal TransductionCell stresschaperones
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TLR2 and Dectin-1 Signaling in Mouse Hematopoietic Stem and Progenitor Cells Impacts the Ability of the Antigen Presenting Cells They Produce to Acti…

2020

Microbial recognition by pattern recognition receptors (PRRs) expressed on hematopoietic stem and progenitor cells (HSPCs) not only activates myelopoiesis but also programs the function of the monocytes and macrophages they produce. For instance, changes in HSPC programming modify the ability of macrophages derived from them to produce inflammatory cytokines. While HSPCs exposed to a TLR2 agonist give rise to tolerized macrophages (lower proinflammatory cytokine production), HSPCs treated with Dectin-1 ligands produce trained macrophages (higher proinflammatory cytokine production). However, nothing is known about the impact of HSPC exposure to microbes on the function of antigen presenting…

CD4-Positive T-LymphocytesOvalbuminhematopoietic stem and progenitor cellsCD4 T cellsAntigen-Presenting CellsMice Transgenicantigen presenting cellsLymphocyte Activationinnate immune memoryProinflammatory cytokineLipopeptidesCandida albicansAnimalsTLR2Lectins C-TypeProgenitor cellAntigen-presenting celllcsh:QH301-705.5CD86CD40biologyChemistryCommunicationHistocompatibility Antigens Class IIZymosanGeneral MedicineTh1 CellsHematopoietic Stem CellsAcquired immune systemToll-Like Receptor 2Cell biologyMice Inbred C57BLlcsh:Biology (General)biology.proteinCytokinesTh17 CellsMyelopoiesisCD80Dectin-1Signal TransductionCells
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Risk perception and gratitude mediate the negative relationship between COVID-19 management satisfaction and public anxiety

2023

AbstractIn this study, we explored whether satisfaction with government management, perception of risk, and gratitude influenced public anxiety during the COVID-19 pandemic in China. Using a cross-sectional, anonymous and confidential online survey, a nationwide sample of Chinese adults (N = 876) was targeted between March 25–March 30, 2020, a period in which newly confirmed cases significantly declined in China. The anxiety level was decreased as compared to that assessed during the peak period. Multiple parallel mediation modeling demonstrated that risk perception and gratitude partially mediated the relationship between satisfaction with government management and public anxiety. Increasi…

COVID-19 pandemicsattitudeskiitollisuusMultidisciplinaryterveyspolitiikkagovernmentCOVID-19asenteetgratitudemental well-beinganxietypandemiathallintotoimethenkinen hyvinvointimielenterveystunteetKiinaahdistusjulkinen hallintoScientific Reports
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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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Pharmacogenomics: a tool to prevent and cure coronary heart disease.

2007

Inflammation and genetics play an important role in the pathogenesis of coronary heart disease (CHD). This is supported by epidemiological studies which have thoroughly investigated the association between CHD and gene polymorphisms of the inflammatory molecules. Moreover, efforts to find elective therapy have not been rewarding and, despite the increasing appreciation of the role of genetics in CHD and myocardial infarction (MI) pathogenesis, pharmacogenomic approaches to uncover drug target have not been extensively explored. A critical search of published literature has suggested few inflammatory genes directly involved in the risk to develop CHD and MI. The selected genes are, the pro- …

Candidate genepharmacogenomicLipoxygenaseLipopolysaccharide ReceptorsMyocardial InfarctionCoronary DiseaseDiseaseBioinformaticsRisk AssessmentPathogenesisRisk FactorsDrug DiscoverymedicinecytokineHumansGenetic Predisposition to DiseaseMyocardial infarctionTLR4PharmacologyInflammationPolymorphism Geneticbusiness.industryPatient SelectionCase-control studyCOXLOXmedicine.diseaseAtherosclerosisToll-Like Receptor 4Treatment OutcomePharmacogeneticsProstaglandin-Endoperoxide SynthasesPharmacogenomicsCase-Control StudiesImmunologyCytokinesReceptors ChemokineChemokinesbusinessRisk assessmentCD14CCR5PharmacogeneticsCurrent pharmaceutical design
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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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IgG1 B cell receptor signaling is inhibited by CD22 and promotes the development of B cells whose survival is less dependent on Ig alpha/beta.

2007

We describe a mouse strain in which B cell development relies either on the expression of membrane-bound immunoglobulin (Ig) gamma1 or mu heavy chains. Progenitor cells expressing gamma1 chains from the beginning generate a peripheral B cell compartment of normal size with all subsets, but a partial block is seen at the pro- to pre-B cell transition. Accordingly, gamma1-driven B cell development is disfavored in competition with developing B cells expressing a wild-type (WT) IgH locus. However, the mutant B cells display a long half-life and accumulate in the mature B cell compartment, and even though partial truncation of the Ig alpha cytoplasmic tail compromises their development, it does…

Cell SurvivalCellular differentiationSialic Acid Binding Ig-like Lectin 2ImmunologyNaive B cellB-cell receptorImmunoglobulinsReceptors Antigen B-CellBiologyArticle03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsProgenitor cellMemory B cellB cell030304 developmental biologyCell ProliferationMice Knockout0303 health sciencesB-LymphocytesCell growthCD22Toll-Like ReceptorsCell DifferentiationArticlesMolecular biologyCell biologyMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GMutationCalciumDimerizationCD79 AntigensSpleen030215 immunologyProtein BindingSignal TransductionThe Journal of experimental medicine
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Herpes virus entry mediator synergizes with Toll-like receptor mediated neutrophil inflammatory responses

2006

In microbial infections polymorphnuclear neutrophils (PMN) constitute a major part of the innate host defence, based upon their ability to rapidly accumulate in inflamed tissues and clear the site of infection from microbial pathogens by their potent effector mechanisms. The recently described transmembrane receptor herpes virus entry mediator (HVEM) is a member of the tumour necrosis factor receptor super family and is expressed on many haematopoietic cells, including T cells, B cells, natural killer cells, monocytes and PMN. Interaction of HVEM with the natural ligand LIGHT on T cells has a costimulatory effect, and increases the bactericidal activity of PMN. To further characterize the f…

Cell SurvivalNeutrophilsImmunologyInflammationBiologyLigandsCell DegranulationNeutrophil ActivationPhagocytosismedicineHumansImmunology and AllergyOpsoninCells CulturedRespiratory BurstToll-like receptorInnate immune systemEffectorInterleukin-8Toll-Like ReceptorsDegranulationOriginal ArticlesAcquired immune systemRespiratory burstCell biologyImmunologyInflammation Mediatorsmedicine.symptomReceptors Tumor Necrosis Factor Member 14Immunology
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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