Search results for "coculture"

showing 10 items of 187 documents

Human dendritic cells transfected with allergen-DNA stimulate specific immunoglobulin G4 but not specific immunoglobulin E production of autologous B…

2007

Atopic/allergic diseases are characterized by T helper 2 (Th2)-dominated immune responses resulting in immunoglobulin E (IgE) production. DNA-based immunotherapies have been shown to shift the immune response towards Th1 in animal models. In further studies we showed that human dendritic cells (DC) transfected with allergen-DNA are able to stimulate autologous CD4(+) T cells from atopic individuals to produce Th1 instead of Th2 cytokines and to activate interferon-gamma (IFN-gamma)-producing CD8(+) T cells. The aim of this study was to analyse whether DC transfected with allergen-DNA are also able to influence immunoglobulin production of B cells from atopic donors. For this purpose, human …

CD4-Positive T-LymphocytesHypersensitivity ImmediateAllergyImmunologyCD8-Positive T-Lymphocytesmedicine.disease_causeImmunoglobulin ELymphocyte ActivationTransfectionAllergenImmune systemmedicineImmunology and AllergyHumansCells CulturedCell ProliferationPlant ProteinsRhinitisB-LymphocytesCD40biologyTransfectionOriginal ArticlesDendritic CellsAllergensImmunoglobulin ETh1 Cellsmedicine.diseaseCoculture TechniquesImmunoglobulin GImmunologybiology.proteinCytokinesAntibodyCD8T-Lymphocytes Cytotoxic
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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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CD4(+) and CD8(+) anergic T cells induced by interleukin-10-treated human dendritic cells display antigen-specific suppressor activity.

2002

Interleukin-10 (IL-10)–treated dendritic cells (DCs) induce an alloantigen- or peptide-specific anergy in various CD4+ and CD8+ T-cell populations. In the present study, we analyzed whether these anergic T cells are able to regulate antigen-specific immunity. Coculture experiments revealed that alloantigen-specific anergic CD4+ and CD8+ T cells suppressed proliferation of syngeneic T cells in a dose-dependent manner. The same effect was observed when the hemagglutinin-specific CD4+T-cell clone HA1.7 or tyrosinase-specific CD8+ T cells were cocultured with anergic T cells of the same specificity. Anergic T cells did not induce an antigen-independent bystander inhibition. Suppression was depe…

CD4-Positive T-LymphocytesIsoantigensImmunoconjugatesImmunologyAntigen-Presenting Cellschemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesLymphocyte ActivationBiochemistryT-Lymphocytes RegulatoryAbataceptInterleukin 21Antigens CDAntigens NeoplasmCytotoxic T cellHumansCTLA-4 AntigenIL-2 receptorLeukapheresisAntigen-presenting cellMelanomaCells CulturedClonal AnergyImmunosuppression TherapyMonophenol MonooxygenaseCD28Cell BiologyHematologyDendritic cellT lymphocyteDendritic CellsNatural killer T cellAntigens DifferentiationCoculture TechniquesCell biologyInterleukin-10ImmunologyCD4 AntigensLeukocytes MononuclearCell DivisionBlood
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Blue light irradiation suppresses dendritic cells activationin vitro

2013

Blue light is a UV-free irradiation suitable for treating chronic skin inflammation, for example, atopic dermatitis, psoriasis, and hand- and foot eczema. However, a better understanding of the mode of action is still missing. For this reason, we investigated whether dendritic cells (DC) are directly affected by blue light irradiation in vitro. Here, we report that irradiation neither induced apoptosis nor maturation of monocyte-derived and myeloid DC. However, subsequent DC maturation upon LPS/IFNγ stimulation was impaired in a dose-dependent manner as assessed by maturation markers and cytokine release. Moreover, the potential of this DC to induce cytokine secretion from allogeneic CD4 T …

CD4-Positive T-LymphocytesLipopolysaccharidesLightUltraviolet Raysmedicine.medical_treatmentStimulationInflammationCell SeparationDermatologyLymphocyte ActivationBiochemistryInterferon-gammaPsoriasismedicineHumansIrradiationMolecular BiologyImmunosuppression TherapyInflammationChemistryDendritic Cellsmedicine.diseaseCoculture TechniquesIn vitroCell biologyCytokineApoptosisImmunologyCytokinesCytokine secretionmedicine.symptomExperimental Dermatology
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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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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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Dendritic Cells Lose Ability to Present Protein Antigen after Stimulating Antigen-Specific T Cell Responses, despite Upregulation of MHC Class II Exp…

2000

Abstract Immature dendritic cells (DC) take up, process and present protein antigens; mature DC are specialized for stimulating primary T cell responses with increased expression of MHC class II and co-stimulatory molecules, but are incapable of processing and presenting soluble protein. The current study examined whether maturation of DC is triggered by T cell recognition of antigens presented by immature DC. Human DC derived from CD34+ progenitor cells by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-6 (IL-6) in serum-free medium could prime naive CD4+ T cells to keyhole limpet hemocyanin (KLH) and ovalbumin (OVA). The cultured DC retained the abil…

CD4-Positive T-LymphocytesTime FactorsOvalbuminT cellImmunologyCD1Bone Marrow CellsCell CommunicationCulture Media Serum-FreeInterferon-gammaInterleukin 21medicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorCD40 AntigensAntigen-presenting cellCells CulturedAntigen PresentationMHC class IIbiologyInterleukin-6Tumor Necrosis Factor-alphaHistocompatibility Antigens Class IIGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationDendritic CellsHematologyIntercellular Adhesion Molecule-1Natural killer T cellMolecular biologyCoculture Techniquesmedicine.anatomical_structureHemocyaninsB7-1 Antigenbiology.proteinImmunobiology
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Monitoring of anti-vaccine CD4 T cell frequencies in melanoma patients vaccinated with a MAGE-3 protein.

2005

Abstract Quantitative evaluation of T cell responses of patients receiving antitumoral vaccination with a protein is difficult because of the large number of possible HLA-peptide combinations that could be targeted by the response. To evaluate the responses of patients vaccinated with protein MAGE-3, we have developed an approach that involves overnight stimulation of blood T cells with autologous dendritic cells loaded with the protein, sorting by flow cytometry of the T cells that produce IFN-γ, cloning of these cells, and evaluation of the number of T cell clones that secrete IFN-γ upon stimulation with the Ag. An important criterion is that T cell clones must recognize not only stimulat…

CD4-Positive T-Lymphocytesmedicine.medical_treatmentT cellImmunologyAntigen presentationMolecular Sequence DataCD4 T cellsCell SeparationBiologyLymphocyte ActivationCancer VaccinesFlow cytometryInterleukin 21Interferon-gammaAntigenSDG 3 - Good Health and Well-beingAntigens NeoplasmMonitoring ImmunologicmedicineTumor Cells CulturedImmunology and AllergyHumansAmino Acid SequenceLymphocyte CountMelanomaCell Line TransformedAntigen Presentationmedicine.diagnostic_testT-cell receptorCoculture TechniquesGrowth InhibitorsClone CellsNeoplasm Proteinsmedicine.anatomical_structureCell cultureImmunologyAdjuvantVaccineMAGE-3 proteinJournal of immunology (Baltimore, Md. : 1950)
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Glioblastoma cells induce differential glutamatergic gene expressions in human tumor-associated microglia/macrophages and monocyte-derived macrophages

2015

Glioblastoma cells produce and release high amounts of glutamate into the extracellular milieu and subsequently can trigger seizure in patients. Tumor-associated microglia/macrophages (TAMs), consisting of both parenchymal microglia and monocytes-derived macrophages (MDMs) recruited from the blood, are known to populate up to 1/3 of the glioblastoma tumor environment and exhibit an alternative, tumor-promoting and supporting phenotype. However, it is unknown how TAMs respond to the excess extracellular glutamate in the glioblastoma microenvironment. We investigated the expressions of genes related to glutamate transport and metabolism in human TAMs freshly isolated from glioblastoma resecti…

Cancer ResearchAntigens Differentiation MyelomonocyticGlutamic AcidglutamateAMPA receptorSLC7A11Antigens CDTumor Cells CulturedExtracellularmedicineHumansReceptors AMPAGRIA2PharmacologyCD11b AntigenbiologyMicrogliaBrain NeoplasmsMacrophagesmonocyte-derived macrophagesCalcium-Binding ProteinsMicrofilament Proteinsglioblastomatumor-associated microglia/macrophagesGlutamate receptorSLC1A2Coculture TechniquesDNA-Binding ProteinsGlutaminemedicine.anatomical_structureGene Expression RegulationOncologyAstrocytesImmunologybiology.proteinCancer researchLeukocyte Common AntigensMolecular MedicineMicrogliaResearch PaperCancer Biology & Therapy
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