Search results for "script"

showing 10 items of 5143 documents

Neuronal nitric oxide synthase modulates maturation of human dendritic cells.

2010

AbstractDendritic cells (DCs) are the most potent APCs of the immune system. Understanding the intercellular and intracellular signaling processes that lead to DC maturation is critical for determining how these cells initiate T cell-mediated immune processes. NO synthesized by the inducible NO synthase (iNOS) is important for the function of murine DCs. In our study, we investigated the regulation of the arginine/NO-system in human monocyte-derived DCs. Maturation of DCs induced by inflammatory cytokines (IL-1β, TNF, IL-6, and PGE2) resulted in a pronounced expression of neuronal NOS (nNOS) but only minimal levels of iNOS and endothelial NOS were detected in human mature DCs. In addition, …

T cellCellular differentiationImmunologyImmunoblottingchemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayCell SeparationNitric Oxide Synthase Type IBiologyEndothelial NOSLymphocyte ActivationNitric OxideProinflammatory cytokineCell LineImmune systemmedicineImmunology and AllergyHumansAutocrine signallingMHC class IIReverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritic CellsFlow CytometryCell biologymedicine.anatomical_structureCell culturebiology.proteinCytokinesJournal of immunology (Baltimore, Md. : 1950)
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Quantitation of antigen-reactive T cells in peripheral blood by IFNgamma-ELISPOT assay and chromium-release assay: a four-centre comparative trial

2000

The ELISPOT assay is increasingly being used for the monitoring of the induction of antigen-reactive T cells in cancer vaccination trials. In order to evaluate the reliability of T cell frequency analysis with the ELISPOT assay, a comparative study was performed in four European laboratories. Six samples from healthy subjects were analyzed for the frequency of influenza-reactive CD8+ T cells in peripheral blood mononuclear cells (PBMC) by IFNgamma-ELISPOT assay. In addition, one laboratory determined cytotoxic T cell precursor (CTL) frequencies in these samples by limiting dilution chromium-release assay (LDA), and three laboratories performed a variant of the LDA, the multiple microculture…

T cellImmunologyEpitopes T-LymphocyteIndicator Dilution TechniquesEnzyme-Linked Immunosorbent AssayCD8-Positive T-LymphocytesLymphocyte ActivationPeripheral blood mononuclear cellViral Matrix ProteinsInterferon-gammaAntigenHLA-A2 AntigenHumansImmunology and AllergyCytotoxic T cellMedicineAntigens ViralImmunodominant Epitopesbusiness.industryELISPOTMolecular biologyChromium RadioisotopesHIV Reverse TranscriptasePeptide FragmentsCTL*medicine.anatomical_structureImmunologyLeukocytes MononuclearCancer vaccinebusinessCD8T-Lymphocytes Cytotoxic
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CD4 blockade directly inhibits mouse and human CD4+ T cell functions independent of Foxp3+ Tregs

2013

CD4(+) helper T cells orchestrate protective immunity against pathogens, yet can also induce undesired pathologies including allergies, transplant rejection and autoimmunity. Non-depleting CD4-specific antibodies such as clone YTS177.9 were found to promote long-lasting T cell tolerance in animal models. Thus, CD4 blockade could represent a promising therapeutic approach for human autoimmune diseases. However, the mechanisms underlying anti-CD4-induced tolerance are incompletely resolved. Particularly, multiple immune cells express CD4 including Foxp3(+) regulatory T cells (Tregs) and dendritic cells (DCs), both controlling the activation of CD4(+)Foxp3(-) helper T cells. Utilizing mixed le…

T cellImmunologyPriming (immunology)Ki-1 Antigenchemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesLymphocyte ActivationT-Lymphocytes RegulatoryLymphocyte DepletionInterleukin 21MiceImmune systemmedicineImmune ToleranceImmunology and AllergyCytotoxic T cellAnimalsHumansIL-2 receptorCells CulturedAntilymphocyte SerumCell ProliferationMice Inbred BALB CFOXP3Forkhead Transcription Factorshemic and immune systemsDendritic CellsReceptors OX40medicine.diseaseTransplant rejectionMice Inbred C57BLmedicine.anatomical_structureImmunologyCD4 AntigensInterleukin-2
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T helper cell polarisation in coeliac disease: any (T-)bet ?

2004

Recent data strongly support the view that coeliac disease is a Th1 mediated inflammatory disease as both interferon γ production and T-bet levels in gut infiltrating cells are upregulated The puzzling observation on high interferon γ (IFN-γ) but low interleukin (IL)-12 levels in coeliac disease (CD) has resulted in questions about the underlying principles of T helper cell polarisation. In this issue of G ut ,1 the molecular basis of T helper cell polarisation in CD has been illuminated by the finding that T-bet, the master transcription factor of T helper cell type 1 (Th1) cells, is upregulated in this disease [see page 1090] . The past decade has witnessed a dramatic improvement in our p…

T cellInterleukinsGastroenterologyT helper cellCoeliac DiseaseBiologyTh1 CellsGliadinUp-RegulationInterleukin 21Celiac DiseaseInterferon-gammaImmune systemmedicine.anatomical_structureInterleukin 25ImmunologyInterleukin 13medicineCytotoxic T cellCytokinesHumansIL-2 receptorT-Box Domain ProteinsTranscription FactorsGut
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STAT3 activation: A key factor in tumor immunoescape.

2012

Cancer growth is controlled by cancer cells (cell intrinsic phenomenon), but also by the immune cells in the tumor microenvironment (cell extrinsic phenomenon). Thus cancer progression is mediated by the activation of transcription programs responsible for cancer cell proliferation, but also induced proliferation/activation of immunosuppressive cells such as Th17, Treg or myeloid derived suppressor cells (MDSCs). One of the key transcription factors involved in these pathways is the signal transducer and activator of transcription 3 (STAT3). In this review we will focus on STAT3 activation in immune cells, and how it impacts on tumor progression.

T helpersMDSCReviewimmune responseSTAT3Immune systemMedicinecancerdendritic cellsSTAT3Transcription factorTumor microenvironmentbiologybusiness.industryGeneral MedicinemacrophagesTregTumor progressionCancer cellImmunologyMyeloid-derived Suppressor CellSTAT proteinbiology.proteinCancer researchTh17businessJAK-STAT
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Inhibition of Transcription Factors by Plant-Derived Compounds and their Implications in Inflammation and Cancer

2009

Inflammation is a general term used to describe various pathological processes with diverse causes that can include infection, trauma, or an autoimmune response. Due to its many causes, the inflammatory response involves multiple and varied mediators, including vasoactive amines, free radicals, and both lipidic and peptidic mediators. Medicinal plants and the compounds derived from them are a good source of new and specific inhibitors of the inflammatory process. The past decade has witnessed many important discoveries in this field, with new findings challenging the more traditional views of pharmacologists. Various studies, for example, have demonstrated the positive effects of plant-deri…

T-LymphocytesAnti-Inflammatory AgentsArthritisAntineoplastic AgentsInflammationPharmacologychemistry.chemical_compoundDrug DiscoverymedicineAnimalsHumansTranscription factorJanus KinasesPharmacologyNatural productbiologyNF-kappa BJAK-STAT signaling pathwayBiological activityPlantsmedicine.diseasechemistryBiochemistrybiology.proteinCyclooxygenaseSignal transductionmedicine.symptomSignal TransductionTranscription FactorsCurrent Pharmaceutical Design
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An innate cell-mediated, murine ulcerative colitis-like syndrome in the absence of nuclear factor of activated T cells.

2004

Abstract Background & Aims: Nuclear factor of activated T cells transcription factors plays a central role in immunity by regulating the expression of multiple cytokines and other regulatory molecules, many of which have been heavily implicated in the pathogenesis of inflammatory bowel disease. However, few studies have directly investigated the nuclear factor of activated T cells proteins in inflammatory bowel disease. We describe here a specific role for nuclear factor of activated T cells c2 in the pathogenesis of murine inflammatory bowel disease. Methods: Mice deficient for nuclear factor of activated T cells c2, recombinase activating gene-2, or both and transgenic or nontransgenic fo…

T-LymphocytesBiologyInterleukin 21MicemedicineImmune ToleranceCytotoxic T cellAnimalsIL-2 receptorB-LymphocytesImmunity CellularMice Inbred BALB CHepatologyNFATC Transcription FactorsZAP70Innate lymphoid cellGastroenterologyNuclear ProteinsT helper cellRectal ProlapseNatural killer T cellAcquired immune systemMice Mutant StrainsDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureImmunologyCancer researchColitis UlcerativeTranscription FactorsGastroenterology
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NFATc1 affects mouse splenic B cell function by controlling the calcineurin–NFAT signaling network

2011

Mouse B cells lacking NFATc1 exhibit defective proliferation, survival, isotype class switching, cytokine production, and T cell help.

T-LymphocytesImmunologyNaive B cellB-cell receptorReceptors Antigen B-CellLymphocyte ActivationArticleMice03 medical and health sciences0302 clinical medicinemedicineAnimalsImmunology and AllergyB cell030304 developmental biologyB-Lymphocytes0303 health sciencesCD40NFATC Transcription Factorsintegumentary systembiologyCalcineurinCD22Germinal centerImmunoglobulin Class SwitchingMolecular biology3. Good healthB-1 cellCalcineurinmedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchbiology.proteinCalciumSpleenSignal TransductionJournal of Experimental Medicine
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Diacylglycerol-containing oleic acid induces increases in [Ca(2+)](i) via TRPC3/6 channels in human T-cells.

2011

Though most of the studies have focused on the effects of free fatty acids on T-cell activation, fatty acids incorporated into plasma membrane phospholipids may also affect cell signaling via diacylglycerol (DAG), generally produced by phospholipid hydrolysis. In the present study, we have synthesized a DAG-containing oleic acid and studied its implication in the modulation of calcium signaling in human Jurkat T-cells. 1-palmitoyl-2-oleoyl-sn-glycerol (POG) induced a dose-dependent increase in [Ca(2+)](i). This effect was due to the presence of oleic acid at the sn-2 position as no differences were observed between POG and 1-stearoly-2-oleoyl-sn-glycerol (SOG). However, the substitution of …

T-LymphocytesPhospholipidGene ExpressionBiologyCaveolaeDiglycerideschemistry.chemical_compoundJurkat CellsTRPC3Membrane MicrodomainsTRPC6 Cation ChannelHumansCalcium SignalingMolecular BiologyLipid raftCalcium signalingDiacylglycerol kinaseTRPC Cation ChannelsIon TransportVoltage-dependent calcium channelDose-Response Relationship DrugReverse Transcriptase Polymerase Chain Reactionbeta-CyclodextrinsCell BiologyOleic acidchemistryBiochemistryMicroscopy Fluorescencelipids (amino acids peptides and proteins)Arachidonic acidCalciumRNA InterferenceBiochimica et biophysica acta
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Inefficient Termination of Antigen Responses in NF-ATp-Deficient Mice

1998

In order to elucidate the role of NF-ATp, one of the most prominent members of family of NF-AT transcription factors in peripheral T lymphocytes, in T cell activation and differentiation we created NF-ATp-deficient mice by gene targeting. Such NF-ATp-/- mice are born and appear to develop a normal immune system. Apart from clear-cut defects in the synthesis of mRNAs for Th2-type lymphokines, such as IL-4, IL-5, IL-10 and IL-13, in primary and secondary stimulations of spleen cells in vitro, of a distinct impaired deletion of V beta 11+/CD4+ T lymphocytes from these mice was detected after superantigen injection. Moreover, NF-ATp-/- mice older than 6 weeks show an 2-5 fold increase in number…

T-LymphocytesT cellImmunologyApoptosisCell CountEnterotoxinsMiceImmune systemAntigenSuperantigenmedicineAnimalsHumansImmunology and AllergyCell Line TransformedB-LymphocytesLymphokinesSuperantigensNFATC Transcription FactorsbiologyCD44LymphokineNuclear ProteinsGene targetingHematologyMolecular biologyDNA-Binding Proteinsmedicine.anatomical_structureCell culturebiology.proteinGene DeletionTranscription FactorsImmunobiology
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