Search results for "G cell"

showing 10 items of 456 documents

Human parvovirus B19 induced apoptotic bodies contain altered self-antigens that are phagocytosed by antigen presenting cells.

2013

Human parvovirus B19 (B19V) from the erythrovirus genus is known to be a pathogenic virus in humans. Prevalence of B19V infection has been reported worldwide in all seasons, with a high incidence in the spring. B19V is responsible for erythema infectiosum (fifth disease) commonly seen in children. Its other clinical presentations include arthralgia, arthritis, transient aplastic crisis, chronic anemia, congenital anemia, and hydrops fetalis. In addition, B19V infection has been reported to trigger autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. However, the mechanisms of B19V participation in autoimmunity are not fully understood. B19V induced chronic dise…

Programmed cell deathScienceAntigen-Presenting CellsArthritisApoptosisAutoimmunitySpodopteraViral Nonstructural ProteinsBiologymedicine.disease_causeAutoantigensVirusautoimmuniteettiImmune toleranceAutoimmunityParvoviridae InfectionsPathogenesis03 medical and health sciences0302 clinical medicineImmune systemPhagocytosisImmune ToleranceParvovirus B19 HumanSf9 CellsHuman Parvovirus B19medicineta319AnimalsHumansAntigen-presenting cellself-antigens030304 developmental biology0303 health sciencesMultidisciplinaryQta1182RHep G2 CellsFlow Cytometrymedicine.diseaseVirology3. Good healthImmunologyMicroscopy Electron ScanningMedicineResearch Article030215 immunologyPLoS ONE
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Processing without proteolytic cleavage is required for recognition of insulin by T cells.

1990

Beef insulin as well as a chymotryptic A-chain fragment [BI-A1-14(SSO3-)3] need uptake by antigen-presenting cells (APC) for efficient presentation in combination with major histocompatibility complex class II molecules to insulin-specific T cells. This could be shown by the inability of aldehyde-fixed APC to present these antigens to T cells. Furthermore, presentation of the insulin fragment as well as presentation of ovalbumin (OVA) was inhibited by treatment of APC with chloroquine, cerulenin or tunicamycin. This was not the case for a processing-independent OVA peptide. Treatment of APC during antigen pulsing with various protease inhibitors, active on all classes of proteases, did not …

ProteasesOvalbuminmedicine.medical_treatmentT-LymphocytesImmunologyAntigen presentationAntigen-Presenting CellsBiologyIn Vitro TechniquesEpitopeCell Linechemistry.chemical_compoundMiceAntigenEndopeptidasesmedicineImmunology and AllergyAnimalsInsulinProtease InhibitorsAntigen-presenting cellProteaseInsulinTunicamycinChloroquineTunicamycinEndocytosischemistryBiochemistryEuropean journal of immunology
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Processing requirements for the recognition of insulin fragments by murine T cells.

1988

In this study we investigated aspects of antigen processing using insulin and insulin A chain-derived fragments as model antigens in Ab alpha Ak beta-restricted T-cell stimulation. Similarly to other proteins, the immunodominant region of insulin recognized by these T cells is limited in size. It is located on the insulin A chain and encompasses a portion of the molecule that is represented faithfully by peptide A1-14(SSO3-)3. Efficient presentation of intact insulin and its entire A chain is dependent on uptake and processing by APC. Whereas peptides stemming from various globular proteins are known to be presented to T cells by APC without requiring processing, this is not the case with A…

Protein Denaturationmedicine.medical_treatmentT-LymphocytesImmunologyReceptors Antigen T-CellAntigen-Presenting CellsPeptideLymphocyte ActivationMajor Histocompatibility Complexchemistry.chemical_compoundEpitopesAntigenmedicineImmunology and AllergyAnimalsInsulinchemistry.chemical_classificationMHC class IIbiologyAntigen processingInsulinT-cell receptorTunicamycinClone CellsRatsBiochemistrychemistrybiology.proteinInsulin processingImmunological reviews
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B7/CD28 costimulation of T cells induces a distinct proteome pattern.

2005

Effective immune strategies for the eradication of human tumors require a detailed understanding of the interaction of tumor cells with the immune system, which might lead to an optimization of T cell responses. To understand the impact of B7-mediated costimulation on T cell activation comprehensive proteome analysis of B7-primed T cell populations were performed. Using this approach we identified different classes of proteins in T cells whose expression is either elevated or reduced upon B7-1- or B7-2-mediated CD28 costimulation. The altered proteins include regulators of the cell cycle and cell proliferation, signal transducers, components of the antigen processing machinery, transporters…

ProteomeT cellT-LymphocytesAntigen presentationStreptamerBiologyLymphocyte ActivationBiochemistryMass SpectrometryAnalytical ChemistryCD28 AntigensAntigens CDCell Line TumorHLA-A2 AntigenmedicineCytotoxic T cellHumansElectrophoresis Gel Two-DimensionalIL-2 receptorAntigen-presenting cellMolecular BiologyCarcinoma Renal CellDNA PrimersBase SequenceZAP70CD28Blood ProteinsPhosphoproteinsKidney NeoplasmsCell biologymedicine.anatomical_structureGene Expression RegulationLeukocytes MononuclearMolecularcellular proteomics : MCP
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In Vitro Phenotypic, Genomic and Proteomic Characterization of a Cytokine-Resistant Murine β-TC3 Cell Line

2012

Type 1 diabetes mellitus (T1DM) is caused by the selective destruction of insulin-producing β-cells. This process is mediated by cells of the immune system through release of nitric oxide, free radicals and pro-inflammatory cytokines, which induce a complex network of intracellular signalling cascades, eventually affecting the expression of genes involved in β-cell survival. The aim of our study was to investigate possible mechanisms of resistance to cytokine-induced β-cell death. To this purpose, we created a cytokine-resistant β-cell line (β-TC3R) by chronically treating the β-TC3 murine insulinoma cell line with IL-1β + IFN-γ. β-TC3R cells exhibited higher proliferation rate and resistan…

ProteomicsAnatomy and Physiologymedicine.medical_treatmentCell Culture Techniqueslcsh:MedicineApoptosisSettore MED/13 - EndocrinologiaMiceEndocrinologyImmune PhysiologyInsulin-Secreting CellsMolecular Cell BiologySOCS3lcsh:ScienceMultidisciplinaryCell DeathDiabetes mellitus cytokines. apoptosis SUMO4 NF-kBCell CycleNF-kappa BGenomicsCell cycleImmunohistochemistryCell biologyPhenotypeCytokineMedicineCytokinesResearch ArticleProgrammed cell deathCell SurvivalImmunologyDown-RegulationBiologyAutoimmune DiseasesCell LineDownregulation and upregulationmedicineAnimalsGene SilencingBiologyCell ProliferationDiabetic EndocrinologyEndocrine PhysiologyCell growthlcsh:RCell cultureApoptosisImmune SystemClinical ImmunologyInsulinomalcsh:QPLoS ONE
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Biological properties of extracellular vesicles and their physiological functions

2015

The authors wish to thank Dr R Simpson and Dr D Taylor for critical reading of the manuscript and acknowledge the Horizon 2020 European Cooperation in Science and Technology programme and its support of our European Network on Microvesicles and Exosomes in Health & Disease (ME-HaD; BM1202 www.cost.eu/COST_Actions/bmbs/Actions/BM1202). In the past decade, extracellular vesicles (EVs) have been recognized as potent vehicles of intercellular communication, both in prokaryotes and eukaryotes. This is due to their capacity to transfer proteins, lipids and nucleic acids, thereby influencing various physiological and pathological functions of both recipient and parent cells. While intensive invest…

ProteomicsCellular distributionMATURE DENDRITIC CELLSReviewReview ArticleUrineEmbryo developmentMonocyteProtein processingVascular biologyFecesVesícules seminalsSYNCYTIOTROPHOBLAST MICROVILLOUS MEMBRANESCell selectionPregnancyT lymphocyteBileCELL-DERIVED EXOSOMESBiogenesisLung lavageUterus fluidInnate immunityMale genital systemlcsh:CytologyMicrovesicleOUTER-MEMBRANE VESICLESBlood clottingprokaryoteEukaryotaExtracellular vesicleRNA analysisCell biologyBloodCerebrospinal fluidLiver metabolismmicrovesicleMorphogenHumanNervous systemCell signalingBreast milkNatural killer cellFisiologiaExtracellular vesiclesExosomelcsh:QH573-671SalivaBiologyBiology and Life SciencesDNAPlantRNA transportCell functionMacrophageMolecular biologyPhysiologyMedizinProteomicsFACTOR PATHWAY INHIBITOReukaryoteProtein glycosylationExtracellular spaceTissue repairEspai extracel·lularReticulocyteSeminal plasmaMesenchymal stem cellAntigen presenting cellSeminal vesiclesNose mucusBiofilmNeutrophilMicroRNAPLANT-MICROBE INTERACTIONSLipidAmnion fluidProkaryotamicroparticleCell interactionCell transporteukaryote exosome extracellular vesicle microparticle microvesicle physiology prokaryoteBone mineralizationMicroorganismHistologyAdaptive immunityMembrane vesicleComputational biologyMembrane receptorBiologyStressCell communicationMast cellMESENCHYMAL STEM-CELLSHUMAN ENDOTHELIAL-CELLSexosomeCytokineSynovial fluidCell BiologyNonhumanIMMUNE-MODULATORY FEATURESReview articleDNA contentphysiologyRNAINTESTINAL EPITHELIAL-CELLSextracellular vesicleBody fluidLectinBiogenesis
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Endurance training damages small airway epithelium in mice.

2007

RATIONALE: In athletes, airway inflammatory cells were found to be increased in induced sputum or bronchial biopsies. Most data were obtained after exposure to cold and dry air at rest or during exercise. Whether training affects epithelial and inflammatory cells in small airways is unknown. OBJECTIVES: To test whether endurance training under standard environmental conditions causes epithelial damage and inflammation in the small airways of mice. METHODS AND MEASUREMENTS: Formalin-fixed, paraffin-embedded lung sections were obtained in sedentary (n = 14) and endurance-trained (n = 16) Swiss mice at baseline and after 15, 30, and 45 days of training. The following variables were assessed (m…

Pulmonary and Respiratory MedicineMalePathologymedicine.medical_specialtyInflammationApoptosisCritical Care and Intensive Care MedicineSettore BIO/09 - FisiologiaEpitheliumEpithelial DamageLeukocyte CountMiceEndurance trainingIntensive carePhysical Conditioning AnimalProliferating Cell Nuclear AntigenmedicineLeukocytesAnimalsBronchitisCell ProliferationBasement membraneLungAerobic exercise bronchial responsivenes methacholine deep inspiration leukotrienesbusiness.industryNF-kappa Brespiratory systemImmunohistochemistryEpitheliumrespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureRespiratory epitheliummedicine.symptombusinessAmerican journal of respiratory and critical care medicine
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Amyloid-Beta Induces Different Expression Pattern of Tissue Transglutaminase and Its Isoforms on Olfactory Ensheathing Cells: Modulatory Effect of In…

2021

Abstract Alzhèimer Disease (AD) is characterized by protein aggregates in the brain, including amyloid-beta (Aβ), a substrate for tissue transglutaminase (TG2). We assessed the effect of full native peptide of Aβ (1–42), the fragments (25–35 and 35–25) on TG2 expression and its isoforms (Long and Short) on mouse Olfactory Ensheathing Cells (OECs). The levels of cytoskeletal proteins, Vimentin and Glial Fibrillary Acid Protein, were also studied. The effect of the pre-treatment with Indicaxanthin on cell viability, total Reactive Oxygen Species, superoxide anion and apoptotic pathway activation was assessed. Since Nestin is co-expressed in pluripotent stem cells with cyclin D1, their levels …

Pyridinestissue transglutaminase; olfactory ensheathing cells; amyloid-beta; oxidative stress; Indicaxanthin; self-renewalApoptosisAmyloid‐betaIndicaxanthinVimentinself-renewallcsh:ChemistryNestinMicechemistry.chemical_compoundProtein IsoformsCyclin D1lcsh:QH301-705.5SpectroscopybiologySuperoxideOpuntiaCell DifferentiationGeneral MedicineOlfactory Bulbamyloid-betaBetaxanthinsComputer Science ApplicationsCell biologyIndicaxanthinAmyloid betaTissue transglutaminase; Olfactory Ensheathing Cells; Amyloid-Beta; oxidative stress; In-dicaxanthin; self-renewalArticleGene Expression Regulation EnzymologicCatalysisInorganic ChemistryCyclin D1Alzheimer DiseaseGTP-Binding ProteinsGlial Fibrillary Acidic ProteinAnimalsHumansVimentinProtein Glutamine gamma Glutamyltransferase 2Viability assayPhysical and Theoretical ChemistryMolecular BiologyAmyloid beta-PeptidesTransglutaminasesOrganic ChemistryTissue transglutaminaseNestinSelf‐renewalNerve Regenerationlcsh:Biology (General)lcsh:QD1-999chemistryOxidative stressOlfactory ensheathing cellsbiology.proteinOlfactory ensheathing gliaReactive Oxygen SpeciesInternational Journal of Molecular Sciences
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Factors that influence the quality of metabolomics data in in vitro cell toxicity studies: a systematic survey

2021

Abstract REACH (Registration, Evaluation, Authorization and Restriction of Chemicals) is a global strategy and regulation policy of the EU that aims to improve the protection of human health and the environment through the better and earlier identification of the intrinsic properties of chemical substances. It entered into force on 1st June 2007 (EC 1907/2006). REACH and EU policies plead for the use of robust high-throughput "omic" techniques for the in vitro investigation of the toxicity of chemicals that can provide an estimation of their hazards as well as information regarding the underlying mechanisms of toxicity. In agreement with the 3R’s principles, cultured cells are nowadays wide…

Quality ControlHEPATOTOXICITYSciencemedia_common.quotation_subjectDiseasesComputational biologyMETABOLISMBiologyHEPATOCYTESCitric AcidArticleXenobioticsProductes químicschemistry.chemical_compoundMetabolomicsMedical researchCell Line TumorMetabolomeHumansMetabolomicsSPECTROMETRY DATAQuality (business)HEPARG CELLSAcetaminophenmedia_commonBATCH EFFECT CORRECTIONMultidisciplinaryFATTY-ACIDDrug discoveryValproic AcidQRReproducibility of ResultsHep G2 CellsIn vitroBioactive compoundGLUTAMINEMetabolic pathwayLiverchemistryToxicityMetabolomeMedicineCURRENT STATEChemical and Drug Induced Liver InjuryXenobioticMetabolic Networks and PathwaysBiomarkersVALPROATEScientific Reports
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EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

2005

Abstract The EBV-induced gene 3 (EBI3) is expressed in dendritic cells (DCs) and part of the cytokine IL-27 that controls Th cell development. However, its regulated expression in DCs is poorly understood. In the present study we demonstrate that EBI3 is expressed in splenic CD8−, CD8+, and plasmacytoid DC subsets and is induced upon TLR signaling. Cloning and functional analysis of the EBI3 promoter using in vivo footprinting and mutagenesis showed that stimulation via TLR2, TLR4, and TLR9 transactivated the promoter in primary DCs via NF-κB and Ets binding sites at −90 and −73 bp upstream of the transcriptional start site, respectively. Furthermore, we observed that NF-κB p50/p65 and PU.1…

RNA Capsmedicine.medical_treatmentDNA Mutational AnalysisMolecular Sequence DataImmunologyAntigen-Presenting CellsReceptors Cell SurfaceBiologyCell LineMinor Histocompatibility AntigensJurkat CellsMiceCell Line TumorGene expressionmedicineAnimalsHumansImmunology and AllergyReceptors CytokinePromoter Regions GeneticGlycoproteinsMice KnockoutMembrane GlycoproteinsInnate immune systemBase SequenceToll-Like ReceptorsHEK 293 cellsNF-kappa BTLR9hemic and immune systemsEBI3Dendritic CellsMolecular biologyToll-Like Receptor 2Up-RegulationMice Inbred C57BLToll-Like Receptor 4Protein SubunitsTLR2CytokineGene Expression RegulationToll-Like Receptor 9NIH 3T3 CellsTLR4Protein BindingSignal TransductionThe Journal of Immunology
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