Search results for " growth factor"

showing 10 items of 1227 documents

A Key Regulatory Role of the Transcription Factor NFATc2 in Bronchial Adenocarcinoma via CD8+ T Lymphocytes

2009

AbstractThe Ca2+-regulated calcineurin/nuclear factor of activated T cells (NFAT) cascade controls alternative pathways of T-cell activation and peripheral tolerance. Here, we describe reduction of NFATc2 mRNA expression in the lungs of patients with bronchial adenocarcinoma. In a murine model of bronchoalveolar adenocarcinoma, mice lacking NFATc2 developed more and larger solid tumors than wild-type littermates. The extent of central tumor necrosis was decreased in the tumors in NFATc2(−/−) mice, and this finding was associated with reduced tumor necrosis factor-α and interleukin-2 (IL-2) production by CD8+ T cells. Adoptive transfer of CD8+ T cells of NFATc2(−/−) mice induced transforming…

CD4-Positive T-LymphocytesCancer ResearchAdoptive cell transferTranscription GeneticTransplantation HeterologousMice TransgenicReceptors Nerve Growth FactorAdenocarcinomaCD8-Positive T-LymphocytesBiologyReceptors Tumor Necrosis FactorTransforming Growth Factor beta1Interferon-gammaMiceGlucocorticoid-Induced TNFR-Related ProteinAnimalsHumansIL-2 receptorInterleukin-7 receptorMice Inbred BALB CReceptors Interleukin-7NFATC Transcription FactorsTumor Necrosis Factor-alphaBronchial NeoplasmsInterleukin-2 Receptor alpha SubunitPeripheral toleranceForkhead Transcription FactorsNFATCalcineurinDisease Models AnimalOncologyCancer researchInterleukin-2Tumor necrosis factor alphaCD8Cancer Research
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Soluble GARP has potent antiinflammatory and immunomodulatory impact on human CD4+ T cells

2013

Glycoprotein A repetitions predominant (GARP) is expressed on the surface of activated human regulatory T cells (Treg) and regulates the bioavailability of transforming growth factor-β (TGF-β). GARP has been assumed to require membrane anchoring. To investigate the function of GARP in more detail, we generated a soluble GARP protein (sGARP) and analyzed its impact on differentiation and activation of human CD4⁺ T cells. We demonstrate that sGARP efficiently represses proliferation and differentiation of naïve CD4⁺ T cells into T effector cells. Exposure to sGARP induces Foxp3, decreases proliferation and represses interleukin (IL)-2 and interferon-γ production, resulting in differentiation …

CD4-Positive T-LymphocytesCellular differentiationBlotting WesternTransplantation HeterologousImmunologyAnti-Inflammatory AgentsGraft vs Host DiseaseApoptosisBiologyReal-Time Polymerase Chain ReactionT-Lymphocytes RegulatoryBiochemistryProinflammatory cytokineInterferon-gammaMiceTransforming Growth Factor betamedicineAnimalsHumansRNA MessengerCells CulturedCell ProliferationInflammationMice KnockoutReverse Transcriptase Polymerase Chain ReactionEffectorInterleukinsMembrane ProteinsInterleukinPeripheral toleranceFOXP3Cell DifferentiationForkhead Transcription FactorsCell BiologyHematologyFlow Cytometrymedicine.diseaseCell biologyTransplant rejectionDNA-Binding ProteinsAnimals NewbornHumanized mouseImmunologyInterleukin-2FemaleSignal TransductionBlood
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Regulatory activity of human CD4 CD25 T cells depends on allergen concentration, type of allergen and atopy status of the donor.

2005

Regulatory CD4+ CD25+ FoxP3-positive T cells (Treg) are functional in most atopic patients with allergic rhinitis and are able to inhibit T helper type 1 (Th1) and Th2 cytokine production of CD4+ CD25- T cells. This study was designed to analyse the following additional aspects: influence of allergen concentration, influence of the type of allergen, and influence of the atopy status of the donor on the strength of the regulatory activity. CD4+ CD25- T cells from healthy non-atopic controls or from grass-pollen-allergic or wasp-venom-allergic donors were stimulated alone or in the presence of Treg with autologous mature monocyte-derived dendritic cells which were pulsed with different concen…

CD4-Positive T-LymphocytesHypersensitivity ImmediateAllergymedicine.medical_treatmentImmunologyDose-Response Relationship Immunologicchemical and pharmacologic phenomenaWasp VenomsReceptors Nerve Growth FactorBiologymedicine.disease_causePoaceaeReceptors Tumor Necrosis FactorAtopyInterleukin 21AllergenTh2 CellsAntigenT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyHumansIL-2 receptorReceptorCells CulturedCell Proliferationhemic and immune systemsForkhead Transcription FactorsReceptors Interleukin-2Original ArticlesAllergensTh1 Cellsmedicine.diseaseCoculture TechniquesCytokineImmunologyCytokinesPollenImmunology
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Cutting Edge: TGF-β Induces a Regulatory Phenotype in CD4+CD25− T Cells through Foxp3 Induction and Down-Regulation of Smad7

2004

Abstract CD4+CD25+ regulatory cells are a subpopulation of T lymphocytes of thymic origin. However, recent data suggest an alternative commitment of regulatory T cells in the periphery, although the precise mechanism is unknown. In the present work, we demonstrate that TGF-β is able to induce Foxp3 expression and subsequently a regulatory phenotype in CD4+CD25− peripheral murine T cells. Similarly, TGF-β induced Foxp3 in human CD4+CD25− T cells. Moreover, we show that the inhibitory Smad7 protein that is normally induced by TGF-β and limits TGF-β signaling, is strongly down-regulated by Foxp3 at the transcriptional level. Foxp3-mediated down-regulation of Smad7 subsequently rendered CD4+CD2…

CD4-Positive T-LymphocytesImmunologyDown-Regulationchemical and pharmacologic phenomenaThymus GlandBiologyImmunophenotypingSmad7 ProteinMiceInterleukin 21Downregulation and upregulationT-Lymphocyte SubsetsTransforming Growth Factor betaTGF beta signaling pathwayAnimalsHumansImmunology and AllergyCytotoxic T cellIL-2 receptorCells CulturedZAP70FOXP3Cell DifferentiationForkhead Transcription FactorsReceptors Interleukin-2hemic and immune systemsPhenotypeCell biologyDNA-Binding ProteinsTrans-ActivatorsSpleenSignal TransductionThe Journal of Immunology
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Hematopoietic Growth Factors Are Differentially Regulated in Monocytes and CD4+T Lymphocytes: Influence of IFN-α and Interleukin-4

1998

We investigated the influence of interferon-alpha (IFN-alpha) on the synthesis of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3) by monocytes and activated T helper cells. IFN-alpha inhibited the production of GM-CSF in unstimulated and lipopolysaccharide (LPS)-activated monocytes to the same extent as was observed in the presence of IL-4. In highly purified CD4+ T cells, which were activated by incubation with immobilized anti-CD3 antibody and anti-CD28, IFN-alpha reduced production of GM-CSF to 47%. In contrast, GM-CSF production in activated T cells was unaffected by exogenously added IL-4. The production of IL-3 by T helper cells was significantly inh…

CD4-Positive T-LymphocytesImmunologyGranulocyte-Macrophage Colony-Stimulating FactorInterferon-alphaT-Lymphocytes Helper-InducerCell BiologyBiologyMonocytesInterferon-gammaInterleukin 21HaematopoiesisTransforming Growth Factor betaVirologyImmunologyHumansCytotoxic T cellInterleukin-3Interleukin-4Cells CulturedInterleukin 4Journal of Interferon & Cytokine Research
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Asthmatic changes in mice lacking T-bet are mediated by IL-13

2005

Mice with a targeted deletion of the T-bet gene exhibit spontaneous airway hyperresponsiveness (AHR), airway inflammation, enhanced recovery of T(h)2 cytokines from bronchoalveolar lavage fluid, sub-epithelial collagen deposition and myofibroblast transformation. Here we analyze the mechanisms responsible for the chronic airway remodeling observed in these mice. CD4+ T cells isolated from the lung of T-bet-deficient mice were spontaneously activated CD44(high)CD69(high) memory T cells, with a typical T(h)2 cytokine profile. Neutralization of IL-13 but not IL-4 resulted in amelioration of AHR in airways of mice lacking T-bet. IL-13 blockade also led to reduced eosinophilia and decreased vime…

CD4-Positive T-LymphocytesImmunologychemical and pharmacologic phenomenaVimentinLymphocyte ActivationSmad7 ProteinMiceTransforming Growth Factor betamedicineAnimalsVimentinImmunology and AllergyEosinophiliaSmad3 ProteinLungCells CulturedMice KnockoutInterleukin-13Lungbiologymedicine.diagnostic_testChemistryCD69hemic and immune systemsGeneral MedicineTransforming growth factor betaFibroblastsrespiratory systemActinsAsthmarespiratory tract diseasesDNA-Binding ProteinsMice Inbred C57BLBronchoalveolar lavagemedicine.anatomical_structureInterleukin 13ImmunologyTrans-Activatorsbiology.proteinCytokinesInterleukin-4medicine.symptomT-Box Domain ProteinsImmunologic MemoryMyofibroblastTranscription FactorsInternational Immunology
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Potential involvement of IL-9 and Th9 cells in the pathogenesis of rheumatoid arthritis

2015

Objective IL-9 has been shown to be upregulated before the clinical onset of articular disease in RA. The exact role of IL-9 and Th9 cells in RA, however, has not yet been adequately studied. The aim of this study was to evaluate the expression of IL-9 and IL-9-expressing cells in RA patients. Methods IL-9, IL-9R, PU.1, IL-9, thymic stromal lymphopoietin (TSLP), IL-4 and TGF-β expression was assessed by real-time-PCR in the synovial tissues of RA and OA patients. IL-9, IL-9R, IL-4, TSLP and TGF-β were also investigated by immunohistochemistry. Peripheral CD4(+) T cell subsets were studied by flow cytometry analysis before and after incubation with citrullinated peptides. Results IL-9 was ov…

CD4-Positive T-LymphocytesMaleCitrullinated peptide; IL-9; Rheumatoid arthritis; Th9 cells; Adolescent; Adult; Arthritis Rheumatoid; CD4-Positive T-Lymphocytes; Cells Cultured; Cytokines; Female; Gene Expression Regulation; Humans; Interleukin-4; Interleukin-9; Lymphocyte Activation; Male; Middle Aged; RNA Messenger; Synovial Membrane; T-Lymphocyte Subsets; Transforming Growth Factor beta; Young Adult; Rheumatology; Medicine (all); Pharmacology (medical)MessengerLymphocyte ActivationArthritis RheumatoidT-Lymphocyte SubsetsTransforming Growth Factor betaRheumatoidTh9 cellPharmacology (medical)Cells CulturedCulturedmedicine.diagnostic_testbiologyMedicine (all)Synovial MembraneMiddle Agedmedicine.anatomical_structureCD4-Positive T-LymphocyteCytokinesFemaleArthritiHumanAdultThymic stromal lymphopoietinAdolescentT cellCD3T-Lymphocyte SubsetCitrullinated peptidePeripheral blood mononuclear cellFlow cytometryYoung AdultRheumatologyThymic Stromal LymphopoietinmedicineHumansInterleukin 9RNA MessengerCytokineInterleukin 4Rheumatoid arthritibusiness.industryInterleukin-9IL-9Settore MED/16 - ReumatologiaGene Expression RegulationImmunologybiology.proteinRNACellInterleukin-4Synovial membranebusiness
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NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells

2005

The phenotype of NFATc2(-/-) c3(-/-) (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4(+) CD25(+) T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) and CD25. However, neither wild-type nor DKO CD4(+) CD25(+) regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4(+) CD25(-) T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4(+) CD25(+) T reg cells but renders c…

CD4-Positive T-LymphocytesT cellImmunologyPopulationchemical and pharmacologic phenomenaReceptors Nerve Growth FactorBiologyLymphocyte ActivationReceptors Tumor Necrosis FactorInterleukin 21MiceT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptoreducationTranscription factorMice Knockouteducation.field_of_studyNFATC Transcription FactorsZAP70Brief Definitive ReportNuclear Proteinshemic and immune systemsReceptors Interleukin-2Molecular biologyCoculture TechniquesDNA-Binding Proteinsmedicine.anatomical_structureTranscription FactorsThe Journal of Experimental Medicine
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Autocrine transforming growth factor- from chronic lymphocytic leukemia-β cells interferes with proliferative T cell signals

1999

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of noncycling B cells in lymphatic and extralymphatic tissues. In the present study we investigated the possible contribution of TGF-beta, as secreted by CLL-B cells, on this low proliferative state. CLL-B cells were shown to express TGF-beta RNA and to release bioactive TGF-beta into culture supernatants. Antibody neutralization of endogenously secreted TGF-beta increased the proliferation of CLL-B cells as cultured in the presence of IL-2 or IL-4 or in direct contact with activated CD4+ T cells. In these culture systems, addition of exogenous TGF-beta downregulated basal and cytokineinduced proliferation of CLL-B cell…

CD4-Positive T-LymphocytesT cellPalatine TonsilImmunologyAntineoplastic AgentsCell CommunicationLymphocyte ActivationInterleukin 21Antigens CDTransforming Growth Factor betahemic and lymphatic diseasesmedicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCells CulturedInterleukin 3B-LymphocytesCD40biologyT-Lymphocytes Helper-InducerHematologyLeukemia Lymphocytic Chronic B-CellCoculture TechniquesCell biologyAutocrine Communicationmedicine.anatomical_structurebiology.proteinInterleukin 12Immunobiology
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MS4A12 is a colon-selective store-operated calcium channel promoting malignant cell processes.

2008

AbstractUsing a data mining approach for the discovery of new targets for antibody therapy of colon cancer, we identified MS4A12, a sequence homologue of CD20. We show that MS4A12 is a cell surface protein. Expression analysis and immunohistochemistry revealed MS4A12 to be a colonic epithelial cell lineage gene confined to the apical membrane of colonocytes with strict transcriptional repression in all other normal tissue types. Expression is maintained upon malignant transformation in 63% of colon cancers. Ca2+ flux analyses disclosed that MS4A12 is a novel component of store-operated Ca2+ entry in intestinal cells. Using RNAi-mediated gene silencing, we show that loss of MS4A12 in LoVo co…

Calcium Channel Blockers/pharmacologyCancer ResearchColorectal cancerColonCalcium Channels/geneticsCell Differentiation/geneticsEpidermal Growth Factor/pharmacologyBiologyRNA Small Interfering/pharmacologyModels BiologicalMalignant transformationEpidermal growth factorCell Line TumormedicineMembrane Proteins/antagonists & inhibitorsHumansGrowth factor receptor inhibitorNeoplasm InvasivenessRNA Small InterferingEpidermal Growth FactorGene Expression ProfilingMembrane ProteinsColonic Neoplasms/geneticsCell DifferentiationApical membranemedicine.diseaseCalcium Channel BlockersColon/metabolismCell biologyChemokines/metabolismProtein Structure TertiaryGene Expression Regulation NeoplasticOncologyCell cultureOrgan SpecificityCancer cellColonic NeoplasmsDisease ProgressionCalcium ChannelsChemokinesA431 cellsCancer research
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