Search results for "interferon"

showing 10 items of 963 documents

In vitro effects of aminobisphosphonates on Vgamma9Vdelta2 T cell activation and differentiation.

2006

In this study we have evaluated the in vitro effects of four different aminobisphosphonates, alendronate, risedronate, neridronate and zoledronate, on Vγ9Vδ2 T cell activation and differentiation. All tested aminobisphosphonates induce an IL-2-dependent activation and expansion of Vγ9Vδ2 T lymphocytes in primary PBMC cultures of healthy donors. Most notably, they also determine a different distribution of Vγ9Vδ2 T cell subsets, with decrease of Tnaive and TCM cells and increase of TEM and TEMRA Vγ9Vδ2 cells, indicating that in vitro treatment with aminobisphosphonates induces Vγ9Vδ2 T lymphocytes to differentiate towards an effector/cytotoxic phenotype. Accordingly, Vγ9Vδ2 T lymphocytes cu…

Cell SurvivalT cellT-LymphocytesImmunologyLymphocyte ActivationPeripheral blood mononuclear cellMonocytesFlow cytometry03 medical and health sciencesInterferon-gamma0302 clinical medicinemedicineImmunology and AllergyCytotoxic T cellHumansCytotoxicityImage CytometryPharmacologymedicine.diagnostic_testBone Density Conservation AgentsDiphosphonatesChemistryEffectorCell DifferentiationFlow CytometryPhenotypeIn vitromedicine.anatomical_structure030220 oncology & carcinogenesisCancer research030215 immunologyInternational journal of immunopathology and pharmacology
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The role of signal transducers and activators of transcription in T inflammatory bowel diseases.

2003

Signal transducers and activators of transcription (STAT) proteins are intracellular effector molecules of cytokine-modulated signaling. On the one hand, they play an important role in hematopoiesis and the development of the human immune system. STAT transcription factors are necessary for embryogenesis and the maintenance of the mammalian immune response. In the adult, STAT signaling is responsible for T-cell polarization toward interferon gamma-secreting Th1 T cells or interleukin 4-producing Th2 cells. On the other hand, these proteins are involved in the regulation of T-cell survival. STAT activation is strongly associated with tyrosine phosphorylation by tyrosine kinases, namely Jak1,…

Cell SurvivalT-LymphocytesGastroenterologyTyrosine phosphorylationBiologyInflammatory Bowel DiseasesstatCell biologyHematopoiesischemistry.chemical_compoundchemistryInterferonImmunologySTAT proteinmedicineTrans-ActivatorsImmunology and AllergyHumansProtein inhibitor of activated STATSignal transductionSTAT4STAT6medicine.drugSignal TransductionInflammatory bowel diseases
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Extracellular Vesicles from Neural Stem Cells Transfer IFN-γ via Ifngr1 to Activate Stat1 Signaling in Target Cells

2014

The idea that stem cell therapies work only via cell replacement is challenged by the observation of consistent intercellular molecule exchange between the graft and the host. Here we defined a mechanism of cellular signaling by which neural stem/precursor cells (NPCs) communicate with the microenvironment via extracellular vesicles (EVs), and we elucidated its molecular signature and function. We observed cytokine-regulated pathways that sort proteins and mRNAs into EVs. We described induction of interferon gamma (IFN-γ) pathway in NPCs exposed to proinflammatory cytokines that is mirrored in EVs. We showed that IFN-γ bound to EVs through Ifngr1 activates Stat1 in target cells. Finally, we…

Cell signalingCell CommunicationBiologyArticle3T3 cellsProinflammatory cytokineInterferon-gammaMiceTh2 CellsNeural Stem CellsPrecursor cellmedicineAnimalsInterferon gammaRNA MessengerTransport VesiclesMolecular BiologyReceptors InterferonInflammationBiological Transport3T3 CellsCell BiologyTh1 CellsNeural stem cellCell biologySTAT1 Transcription Factormedicine.anatomical_structureCellular MicroenvironmentSignal transductionStem cellSignal Transductionmedicine.drugMolecular Cell
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The transcription factor Interferon Regulatory Factor 4 is required for the generation of protective effector CD8 + T cells

2013

Robust cytotoxic CD8 + T-cell response is important for immunity to intracellular pathogens. Here, we show that the transcription factor IFN Regulatory Factor 4 (IRF4) is crucial for the protective CD8 + T-cell response to the intracellular bacterium Listeria monocytogenes . IRF4-deficient ( Irf4 −/− ) mice could not clear L. monocytogenes infection and generated decreased numbers of L. monocytogenes -specific CD8 + T cells with impaired effector phenotype and function. Transfer of wild-type CD8 + T cells into Irf4 −/− mice improved bacterial clearance, suggesting an intrinsic defect of CD8 + T cells in Irf4 −/− mice. Following transfer into wild-type recipients, Irf4 −/− CD8 + T cells bec…

Cellular differentiationGene ExpressionEomesoderminBiologyMiceInterleukin 21AnimalsCytotoxic T cellListeriosisIL-2 receptorAntigen-presenting cellSTAT4Cell ProliferationMice KnockoutMultidisciplinaryCell DifferentiationBiological SciencesListeria monocytogenesMolecular biologyMice Inbred C57BLHost-Pathogen InteractionsInterferon Regulatory FactorsImmunologyPositive Regulatory Domain I-Binding Factor 1CD8T-Lymphocytes CytotoxicTranscription FactorsProceedings of the National Academy of Sciences
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Th9 cells, new players in adaptive immunity.

2014

Upon antigen-specific stimulation, naive CD4⁺ T cells have the potential to differentiate into various T helper (Th) cell subsets. Earlier models of Th cell differentiation focused on IFN-γ-producing Th1 cells and IL-4-secreting Th2 cells. The discovery of additional CD4⁺ Th cell subsets has extended our understanding of Th cell differentiation beyond this dichotomy. Among these is the recently described Th9 cell subset, which preferentially produces interleukin (IL)-9. Here, we review the latest developments in Th9 cell development and differentiation, focusing on contributing environmental signals, and discuss potential physiological and pathophysiological functions of these cells. We des…

Cellular differentiationImmunologyReceptors Antigen T-CellAdaptive ImmunityMiceT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsmedicineHypersensitivityImmunology and AllergyAnimalsHumansInterleukin 9Interleukin 4biologyCell growthLymphocyte differentiationInterleukin-9Models ImmunologicalReceptors Interleukin-2Transforming growth factor betaT helper cellT-Lymphocytes Helper-InducerAcquired immune systemReceptors Interleukin-4medicine.anatomical_structureImmunologyInterferon Regulatory Factorsbiology.proteinSignal TransductionTrends in immunology
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Melanoma-Reactive Class I-Restricted Cytotoxic T Cell Clones Are Stimulated by Dendritic Cells Loaded with Synthetic Peptides, but Fail to Respond to…

2003

Abstract Immunization with heat shock proteins (hsp) isolated from cancer cells has been shown to induce a protective antitumor response. The mechanism of hsp-dependent cellular immunity has been attributed to a variety of immunological activities mediated by hsp. Hsp have been shown to bind antigenic peptides, trim the bound peptides by intrinsic enzymatic activity, improve endocytosis of the chaperoned peptides by APCs, and enhance the ability of APCs to stimulate peptide-specific T cells. We have investigated the potential capacity of hsp70 and gp96 to function as a mediator for Ag-specific CTL stimulation in an in vitro model for human melanoma. Repetitive stimulation of PBLs by autolog…

Cellular immunityT cellImmunologyAntigen-Presenting CellsEpitopes T-LymphocyteBiologyLymphocyte ActivationEpitopeInterferon-gammaMART-1 AntigenAntigenAntigens NeoplasmCell Line TumorHLA-A2 AntigenmedicineHumansImmunology and AllergyCytotoxic T cellHSP70 Heat-Shock ProteinsLymphocyte CountAntigen-presenting cellMelanomaHeat-Shock ProteinsCell Line TransformedAntigen PresentationMonophenol MonooxygenaseDendritic CellsMolecular biologyCoculture TechniquesClone CellsNeoplasm ProteinsUp-RegulationCTL*medicine.anatomical_structureCancer cellK562 CellsPeptidesT-Lymphocytes CytotoxicThe Journal of Immunology
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Cytosolic RIG-I–like helicases act as negative regulators of sterile inflammation in the CNS

2011

The action of cytosolic RIG-I-like helicases (RLHs) in the CNS during autoimmunity is largely unknown. Using a mouse model of multiple sclerosis, we found that mice lacking the RLH adaptor IPS-1 developed exacerbated disease that was accompanied by markedly higher inflammation, increased axonal damage and elevated demyelination with increased encephalitogenic immune responses. Furthermore, activation of RLH ligands such as 5'-triphosphate RNA oligonucleotides decreased CNS inflammation and improved clinical signs of disease. RLH stimulation repressed the maintenance and expansion of committed T(H)1 and T(H)17 cells, whereas T-cell differentiation was not altered. Notably, T(H)1 and T(H)17 s…

Central Nervous SystemEncephalomyelitis Autoimmune ExperimentalCell SurvivalT-LymphocytesAutoimmunityInflammationStimulationReceptor Interferon alpha-betamedicine.disease_causeAutoimmunityMiceCytosolImmune systemmedicineAnimalsbiologyMicrogliaRIG-IGeneral NeuroscienceMultiple sclerosisHelicaseCell DifferentiationDendritic Cellsmedicine.diseasemedicine.anatomical_structurebiology.proteinmedicine.symptomNeuroscienceRNA HelicasesNature Neuroscience
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OTUB1 inhibits CNS autoimmunity by preventing IFN-γ-induced hyperactivation of astrocytes.

2019

Astrocytes are critical regulators of neuroinflammation in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Growing evidence indicates that ubiquitination of signaling molecules is an important cell‐intrinsic mechanism governing astrocyte function during MS and EAE. Here, we identified an upregulation of the deubiquitinase OTU domain, ubiquitin aldehyde binding 1 (OTUB1) in astrocytes during MS and EAE. Mice with astrocyte‐specific OTUB1 ablation developed more severe EAE due to increased leukocyte accumulation, proinflammatory gene transcription, and demyelination in the spinal cord as compared to control mice. OTUB1‐deficient astrocytes were hy…

Central Nervous SystemEncephalomyelitis Autoimmune ExperimentalNeuroimmunomodulationmedicine.medical_treatmentexperimental autoimmune encephalomyelitisAutoimmunityBiologymultiple sclerosisubiquitinationGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineneuroinflammationInterferon-gammaMice03 medical and health sciences0302 clinical medicineastrocytemedicineAnimalsMolecular BiologyCells CulturedNeuroinflammation030304 developmental biologyMice Knockout0303 health sciencesGeneral Immunology and MicrobiologySuppressor of cytokine signaling 1General NeuroscienceExperimental autoimmune encephalomyelitisArticlesmedicine.disease3. Good healthCell biologyMice Inbred C57BLCysteine EndopeptidasesCytokinemedicine.anatomical_structureAnimals NewbornAstrocytesSTAT proteinOTUB1FemaleNeurogenic InflammationJanus kinase030217 neurology & neurosurgeryAstrocyte
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IL-17 and related cytokines involved in the pathology and immunotherapy of multiple sclerosis: Current and future developments.

2014

Multiple sclerosis (MS), an autoimmune neurological disorder, is driven by self-reactive T helper (Th) cells. Research on the role of Th17 lymphocytes in MS pathogenesis has made significant progress in identifying various immunological as well as environmental factors that induce the differentiation and expansion of these cells, different subsets of Th17 cells with varying degrees of pathogenicity, and the role of the secreted effector cytokines. While approved therapies for MS offer significant benefit to patients, there remain unmet needs. Ongoing clinical trials aim to translate the advanced knowledge of Th17 cytokines to improved therapies. This review discusses the current status and …

Central Nervous SystemPathologymedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEndocrinology Diabetes and Metabolismmedicine.medical_treatmentImmunologyAutoimmunityNeurological disorderGeneral Biochemistry Genetics and Molecular BiologyUnmet needsPathogenesisMicemedicineImmunology and AllergyAnimalsHumansEffectorbusiness.industryMultiple sclerosisInterleukin-17Cell DifferentiationImmunotherapyInterferon-betamedicine.diseaseClinical trialImmunologyTh17 CellsInterleukin 17ImmunotherapyInflammation MediatorsbusinessCytokinegrowth factor reviews
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IL-23-mediated mononuclear phagocyte crosstalk protects mice from Citrobacter rodentium-induced colon immunopathology.

2014

Gut homeostasis and mucosal immune defense rely on the differential contributions of dendritic cells (DC) and macrophages. Here we show that colonic CX3CR1+ mononuclear phagocytes are critical inducers of the innate response to Citrobacter rodentium infection. Specifically, the absence of IL-23 expression in macrophages or CD11b+ DC results in the impairment of IL-22 production and in acute lethality. Highlighting immunopathology as a death cause, infected animals are rescued by the neutralization of IL-12 or IFNγ. Moreover, mice are also protected when the CD103+ CD11b− DC compartment is rendered deficient for IL-12 production. We show that IL-12 production by colonic CD103+ CD11b− DC is r…

ChemokineColonCX3C Chemokine Receptor 1General Physics and Astronomychemical and pharmacologic phenomenaMice TransgenicInterleukin-23General Biochemistry Genetics and Molecular BiologyMonocytesArticleMicrobiologyInterferon-gammaMiceIntestinal mucosaAntigens CDImmunopathologyCitrobacter rodentiummedicineAnimalsHomeostasisInterferon gammaIntestinal MucosaImmunity MucosalMultidisciplinaryCD11b AntigenbiologyInterleukinsMacrophagesEnterobacteriaceae InfectionsGeneral ChemistryMononuclear phagocyte systemDendritic CellsInterleukin-12Survival AnalysisImmunity InnateIntegrin alpha MGene Expression RegulationImmunologyInterleukin 12biology.proteinCitrobacter rodentiumTh17 CellsReceptors ChemokineIntegrin alpha Chainsmedicine.drugSignal TransductionNature communications
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