Search results for "signal transduction."

showing 10 items of 1278 documents

LFA-1 Contributes to Signal I of T-Cell Activation and to the Production of Th1 Cytokines

2010

The beta(2) integrins are important for both transendothelial migration of leukocytes and T-cell activation during antigen presentation. In T cells, triggering of leukocyte functional antigen-1 (LFA-1) is required for full activation and T-helper (Th)1/Th2 differentiation. We used CD18-deficient (CD18(-/-)) mice to examine the role of LFA-1 in the activation of T cells. Compared with wild-type controls, CD18(-/-) T cells proliferated normally when stimulated with antibodies against CD3 and CD28, but secreted significantly less IFN-gamma and IL-2 than their wild-type counterparts. However, when T cells were stimulated with dendritic cells (DCs) that provide additional LFA-1 ligation, the pro…

CD3 ComplexT cellchemical and pharmacologic phenomenaDermatologyBiologyBiochemistryAntibodiesMinor Lymphocyte Stimulatory AntigensInterferon-gammaMice03 medical and health sciencesInterleukin 210302 clinical medicineCD28 AntigensCell AdhesionmedicineAnimalsCytotoxic T cellIL-2 receptorAntigen-presenting cellMolecular Biology030304 developmental biologyMice Inbred BALB C0303 health sciencesCD40CD28Cell Differentiationhemic and immune systemsDendritic CellsCell BiologyTh1 CellsIntercellular Adhesion Molecule-1Natural killer T cellLymphocyte Function-Associated Antigen-1Mice Mutant StrainsCell biologyMice Inbred C57BLmedicine.anatomical_structureCD18 Antigensbiology.proteinInterleukin-2Cell DivisionSignal Transduction030215 immunologyJournal of Investigative Dermatology
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Impact of Glutathione Peroxidase-1 Deficiency on Macrophage Foam Cell Formation and Proliferation: Implications for Atherogenesis

2013

Clinical and experimental evidence suggests a protective role for the antioxidant enzyme glutathione peroxidase-1 (GPx-1) in the atherogenic process. GPx-1 deficiency accelerates atherosclerosis and increases lesion cellularity in ApoE(-/-) mice. However, the distribution of GPx-1 within the atherosclerotic lesion as well as the mechanisms leading to increased macrophage numbers in lesions is still unknown. Accordingly, the aims of the present study were (1) to analyze which cells express GPx-1 within atherosclerotic lesions and (2) to determine whether a lack of GPx-1 affects macrophage foam cell formation and cellular proliferation. Both in situ-hybridization and immunohistochemistry of l…

CD36 AntigensMAPK/ERK pathwayMouseMitogen-Activated Protein Kinase 3lcsh:MedicineGene ExpressionSignal transductionCardiovascularMiceMolecular cell biologyGlutathione Peroxidase GPX1lcsh:ScienceIn Situ HybridizationFoam cellMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryReverse Transcriptase Polymerase Chain ReactionKinaseSignaling cascadesScavenger Receptors Class AAnimal ModelsImmunohistochemistryLipoproteins LDLMedicineFemaleSignal transductionResearch ArticleMacrophage colony-stimulating factorMAPK signaling cascadesBlotting WesternBiologyCell GrowthModel OrganismsApolipoproteins EVascular BiologyAnimalsHumansProtein kinase ABiologyCell ProliferationGlutathione PeroxidaseMacrophage Colony-Stimulating Factorlcsh:RAtherosclerosisMolecular biologyMacrophages Peritoneallcsh:QMacrophage proliferationFoam CellsPLoS ONE
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Induction of CD36 and thrombospondin-1 in macrophages by hypoxia-inducible factor 1 and its relevance in the inflammatory process.

2012

Inflammation is part of a complex biological response of vascular tissue to pathogens or damaged cells. First inflammatory cells attempt to remove the injurious stimuli and this is followed by a healing process mediated principally by phagocytosis of senescent cells. Hypoxia and p38-MAPK are associated with inflammation, and hypoxia inducible factor 1 (HIF-1) has been detected in inflamed tissues. We aimed to analyse the role of p38-MAPK and HIF-1 in the transcriptional regulation of CD36, a class B scavenger receptor, and its ligand thrombospondin (TSP-1) in macrophages and to evaluate the involvement of this pathway in phagocytosis of apoptotic neutrophils. We have also assessed HIF-1α, p…

CD36 AntigensMaleAnatomy and PhysiologyNeutrophilsCD36Digestive Physiologylcsh:MedicineApoptosisp38 Mitogen-Activated Protein KinasesBiochemistryMonocytesThrombospondin 1Intestinal mucosaCrohn DiseaseIntestinal Mucosalcsh:ScienceHypoxiaPromoter Regions GeneticMultidisciplinaryProtein StabilityMiddle AgedOxygen Metabolismmedicine.anatomical_structureMedicineFemaleHypoxia-Inducible Factor 1medicine.symptomProtein BindingSignal TransductionResearch ArticleAdultCell PhysiologyAdolescentPhagocytosisImmune CellsImmunologyInflammationGastroenterology and HepatologyBiologyCell LineYoung AdultPhagocytosismedicineHumansUlcerative ColitisScavenger receptorBiologyInflammationLamina propriaDigestive RegulationMacrophageslcsh:RInflammatory Bowel DiseaseHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMetabolismApoptosisImmunologyCancer researchbiology.proteinlcsh:QColitis UlcerativeDigestive SystemPloS one
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Oro-gustatory perception of dietary lipids and calcium signaling in taste bud cells are altered in nutritionally obesity-prone Psammomys obesus.

2013

Since the increasing prevalence of obesity is one of the major health problems of the modern era, understanding the mechanisms of oro-gustatory detection of dietary fat is critical for the prevention and treatment of obesity. We have conducted the present study on Psammomys obesus, the rodent desert gerbil which is a unique polygenic natural animal model of obesity. Our results show that obese animals exhibit a strong preference for lipid solutions in a two-bottle test. Interestingly, the expression of CD36, a lipido-receptor, in taste buds cells (TBC), isolated from circumvallate papillae, was decreased at mRNA level, but remained unaltered at protein level, in obese animals. We further st…

CD36 AntigensMaleTasteAnatomy and PhysiologyCD36BiochemistryCalcium in biologyFatschemistry.chemical_compoundMolecular Cell BiologySignaling in Cellular ProcessesMembrane Receptor Signalingchemistry.chemical_classificationMultidisciplinarybiologyQRTaste PerceptionTaste BudsLipidsSensory SystemsLipid SignalingCytochemistryThapsigarginMedicinePsammomysDisease SusceptibilityIntracellularResearch ArticleSignal Transductionmedicine.medical_specialtyThapsigarginClinical Research DesignLinoleic acidScienceLinoleic AcidFood PreferencesInternal medicinemedicineAnimalsCalcium SignalingObesityAnimal Models of DiseaseBiologyNutritionCell MembraneFatty acidProteinsbiology.organism_classificationLipid MetabolismDietary FatsGustatory SystemTransmembrane ProteinsEndocrinologyMetabolismchemistryGene Expression Regulationbiology.proteinGerbillinaeMembrane CompositionNeurosciencePLoS ONE
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Quercetin ameliorates dysregulation of lipid metabolism genes via the PI3K/AKT pathway in a diet-induced mouse model of nonalcoholic fatty liver dise…

2015

Scope Flavonoids and related compounds seem to have favorable effects on nonalcoholic fatty liver disease (NAFLD) progression, although the exact mechanisms implicated are poorly understood. In this study, we aimed to investigate the effect of the flanovol quercetin on gene expression deregulation involved in the development of NAFLD, as well as the possible implication of phosphatidylinositol 3-kinase (PI3K)/AKT pathway modulation. Methods and results We used an in vivo model based on methionine- and choline-deficient (MCD) diet-fed mice and an in vitro model consisting of Huh7 cells incubated with MCD medium. MCD-fed mice showed classical pathophysiological characteristics of nonalcoholic…

CD36 AntigensMalemedicine.medical_specialtyOxidative phosphorylationBiologyMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseInternal medicineNonalcoholic fatty liver diseaseGene expressionmedicineTranscriptional regulationAnimalsLY294002PhosphatidylinositolCells CulturedPI3K/AKT/mTOR pathwayLipid metabolismLipid Metabolismmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative StressEndocrinologyGene Expression RegulationchemistryCancer researchQuercetinLipid PeroxidationProto-Oncogene Proteins c-aktSignal TransductionFood ScienceBiotechnologyMolecular Nutrition & Food Research
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Activation pattern of signal transducers and activators of transcription (STAT) factors in inflammatory bowel diseases.

2005

Cytokine signaling pathways involving transcription factors of the signal transducers and activators of transcription (STAT) family play a key role in the pathogenesis of inflammatory bowel diseases (IBD). STAT proteins are latent cytoplasmic transcription factors that induce transcription upon phosphorylation, dimerization, and nuclear translocation. However, their activation pattern in IBD is poorly understood. The aim of our study was to characterize STAT-expression in IBD.Mononuclear cells were isolated from 36 colonic specimens of Crohn's disease, ulcerative colitis, or from control patients. Cells were stimulated overnight with antibodies against human CD2 and CD28 and mononuclear cel…

CD4-Positive T-LymphocytesSTAT3 Transcription FactorColonActivation patternstatTranscription (biology)MedicineHumansSTAT4Transcription factorHepatologybusiness.industryActivator (genetics)digestive oral and skin physiologyGastroenterologySTAT2 Transcription FactorSTAT3 Transcription FactorSTAT4 Transcription FactorInflammatory Bowel Diseasesdigestive system diseasesDNA-Binding ProteinsSTAT1 Transcription FactorCase-Control StudiesImmunologyCancer researchTrans-ActivatorsSignal transductionbusinessSTAT6 Transcription FactorThe American journal of gastroenterology
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Local blockade of IL-6R signaling induces lung CD4+ T cell apoptosis in a murine model of asthma via regulatory T cells.

2007

We previously reported high levels of the soluble form of the IL-6R (sIL-6R) in the airways of asthmatic subjects. Here, we analyzed the IL-6R effects on Th2 cell survival in the lung by locally antagonizing sIL-6R-mediated trans-signaling with a designer fusion protein (gp130-Fc) as well as IL-6R signaling with an antibody against the gp80 unit of the IL-6R (alphaIL-6R) in a murine model of asthma after ovalbumin peptide (OVA) sensitization and challenge. Blockade of the sIL-6R led to a significant decrease in inflammatory cells by an apoptosis-independent mechanism. In contrast, local treatment with alphaIL-6R antibodies that also block signaling via the membrane-bound IL-6R (mIL-6R) led …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorOvalbuminT cellRecombinant Fusion ProteinsImmunologyGene ExpressionApoptosisBiologyT-Lymphocytes RegulatoryAntibodiesInterleukin 21MicemedicineCytokine Receptor gp130Immunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPhosphorylationLungMice Inbred BALB CInterleukin-6FOXP3Forkhead Transcription FactorsGeneral MedicineT lymphocyterespiratory systemReceptors Interleukin-6AsthmaCoculture TechniquesImmunoglobulin Fc FragmentsDisease Models Animalmedicine.anatomical_structureApoptosisImmunologyCancer researchFemaleImmunizationSignal transductionBronchoalveolar Lavage FluidSignal TransductionInternational immunology
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Docosahexaenoic acid modulates the expression of T-bet and GATA-3 transcription factors, independently of PPARα, through suppression of MAP kinase ac…

2009

The present study was conducted on CD4(+) T cells, isolated from wild type (WT) and PPARalpha(null) mice, in order to assess the mechanism of action of docosahexaenoic acid (DHA), an n-3 fatty acid, in the modulation of two transcription factors, i.e., T-bet and GATA-3, implicated in T-cell differentiation towards, respectively, T(H)1 and T(H)2 phenotype. The T-cells from PPARalpha(null) mice secreted higher IFN-gamma and lower IL-4 concentrations than WT T-cells. Furthermore, the deletion of PPARalpha gene in T-cells resulted in the upregulation of T-bet and downregulation of GATA-3 both at mRNA and protein levels. DHA exerted not only an inhibitory effect on T-cell proliferation, but also…

CD4-Positive T-LymphocytesTranscriptional ActivationDocosahexaenoic AcidsMAP Kinase Signaling SystemT-LymphocytesCellular differentiationp38 mitogen-activated protein kinasesDown-RegulationPeroxisome proliferator-activated receptorGATA3 Transcription FactorBiologyMitogen-activated protein kinase kinaseBiochemistryInterferon-gammaMiceAnimalsPPAR alphaRNA MessengerPhosphorylationTranscription factorMice Knockoutchemistry.chemical_classificationReverse Transcriptase Polymerase Chain ReactionKinaseCell DifferentiationGeneral MedicineTh1 CellsUp-RegulationCell biologychemistryDocosahexaenoic acidMitogen-activated protein kinaseCancer researchbiology.proteinlipids (amino acids peptides and proteins)Bronchial HyperreactivityMitogen-Activated Protein KinasesT-Box Domain ProteinsSignal TransductionTranscription FactorsBiochimie
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IL-28A Is a Key Regulator of T-Cell–Mediated Liver Injury via the T-Box Transcription Factor T-Bet

2006

Background & Aims: T-cell–mediated fulminant hepatitis is a potentially life-threatening event for which the underlying pathogenic mechanisms are not fully understood. Here, we demonstrate a key regulatory role of IL-28A in T-cell–mediated hepatitis. Methods: We cloned the murine IL-28A gene by reverse-transcription polymerase chain reaction, assessed the effects of recombinant IL-28A, and generated IL-28A–transgenic mice. Results: IL-28A induced TH1 cytokine production by CD4+ T lymphocytes in a T-bet–dependent manner and was up-regulated in a murine model of T-cell–mediated hepatitis upon Con A administration. In vivo, CD4+ T cells from newly created IL-28A–transgenic animals revealed an …

CD4-Positive T-Lymphocytesmedicine.medical_treatmentT cellCodon InitiatorMice TransgenicBiologyAntibodiesProinflammatory cytokineInterferon-gammaMiceT-Lymphocyte SubsetsInterferonConcanavalin AmedicineAnimalsCloning MolecularReceptors CytokineFulminant hepatitisLiver injuryHepatitisHepatologyInterleukinsGastroenterologyLiver Failure AcuteOligonucleotides Antisensemedicine.diseaseMolecular biologyMice Inbred C57BLSTAT1 Transcription FactorReal-time polymerase chain reactionCytokinemedicine.anatomical_structureInterleukin-2Interleukin-4MitogensT-Box Domain ProteinsCell DivisionSignal Transductionmedicine.drugGastroenterology
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β-Catenin Signaling Drives Differentiation and Proinflammatory Function of IRF8-Dependent Dendritic Cells

2014

Abstract β-Catenin signaling has recently been tied to the emergence of tolerogenic dendritic cells (DCs). In this article, we demonstrate a novel role for β-catenin in directing DC subset development through IFN regulatory factor 8 (IRF8) activation. We found that splenic DC precursors express β-catenin, and DCs from mice with CD11c-specific constitutive β-catenin activation upregulated IRF8 through targeting of the Irf8 promoter, leading to in vivo expansion of IRF8-dependent CD8α+, plasmacytoid, and CD103+CD11b− DCs. β-Catenin–stabilized CD8α+ DCs secreted elevated IL-12 upon in vitro microbial stimulation, and pharmacological β-catenin inhibition blocked this response in wild-type cells…

CD8 AntigensCellular differentiationImmunologyReceptors Cell SurfaceVaccinia virusPyrimidinonesCD8-Positive T-LymphocytesBiologyParasite LoadArticleProinflammatory cytokineMiceAntigens CDVacciniaAnimalsImmunology and AllergyPromoter Regions Geneticbeta CateninInflammationMice KnockoutCell DifferentiationDendritic CellsT lymphocyteTh1 CellsBridged Bicyclo Compounds HeterocyclicInterleukin-12CD11c AntigenCell biologyEnzyme ActivationMice Inbred C57BLInterferon Regulatory FactorsInterleukin 12FemaleIRF8Signal transductionIntegrin alpha ChainsToxoplasmaSpleenToxoplasmosisCD8Signal TransductionInterferon regulatory factorsThe Journal of Immunology
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