Search results for "differentiation"

showing 10 items of 1605 documents

Analysis of parathyroid graft rejection suggests alloantigen-specific production of nitric oxide by iNOS-positive intragraft macrophages

2009

Abstract Background During acute rejection of organ or tissue allografts T cells and macrophages are dominant infiltrating cells. CD4-positive T cells are important for the induction of allograft rejection and macrophages are important effector cells mediating cytotoxicity via production of nitric oxide (NO) by the inducible NO-synthase (iNOS). In the present study we analysed whether the destruction of primarily nonvascularised parathyroid allografts is also mediated by iNOS-positive macrophages. Methods Hypocalcaemic Lewis rats received parathyroid isografts (from Lewis donors) and allografts (from Wistar Furth donors), respectively, under the kidney capsule. Levels of serum calcium above…

CD4-Positive T-LymphocytesGraft RejectionMaleImmunologyThyroid GlandNitric Oxide Synthase Type IIRats Inbred WFInflammationCell CommunicationLymphocyte ActivationMajor histocompatibility complexNitric oxidechemistry.chemical_compoundAntigenCell MovementHistocompatibility AntigensmedicineAnimalsTransplantation HomologousImmunology and AllergyCytotoxic T cellMacrophageTransplantationbiologyChemistryMacrophage ActivationAntigens DifferentiationPeptide FragmentsRatsEnzyme ActivationTransplantationMononuclear cell infiltrationGene Expression RegulationRats Inbred LewImmunologyDisease ProgressionMacrophages Peritonealbiology.proteinCalciumImmunizationmedicine.symptomTransplant Immunology
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Direct Cellular Interaction with Activated CD4+T Cells Overcomes Hyporesponsiveness of B-Cell Chronic Lymphocytic Leukemiain Vitro

1998

The proliferative response of clonal B cells from patients with chronic lymphocytic leukemia (B-CLL) is drastically reduced compared to normal B lymphocytes stimulated via the B cell antigen receptor complex or by CD40 ligation. In the present study we demonstrate that hyporesponsiveness of CLL-B cells can be overcome by stimulatory pathways mediated by activated CD4(+) T cells. In contrast to CD40 ligation, costimulation with activated T cells promotes a proliferative response in CLL-B cells identical to that in normal B cells. Furthermore, coculture with activated T cells improved survival of CLL-B cells in vitro. Differentiation of CLL-B cells into IgM producing cells was promoted, as we…

CD4-Positive T-LymphocytesImmunologyB-cell receptorLymphocyte ActivationInterleukin 21Antigens CDhemic and lymphatic diseasesHumansCytotoxic T cellIL-2 receptorCD40 AntigensAntigen-presenting cellCells CulturedB-LymphocytesCD40biologyZAP70Cell DifferentiationLeukemia Lymphocytic Chronic B-CellCell biologyB-1 cellImmunoglobulin MAntigens Surfacebiology.proteinInterleukin-2Cell DivisionCellular Immunology
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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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The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.

2015

The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1β (IL-1β) and IL-18. Whether NLRP3 can shape immunological function independently of inflammasomes is unclear. We found that NLRP3 expression in CD4(+) T cells specifically supported a T helper type 2 (TH2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a TH2 program. In TH2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient TH2 cells supported melanoma tumor growth in an IL-4-dependent manner and …

CD4-Positive T-LymphocytesInflammasomesImmunologyBlotting WesternBiologyInterleukin 21MiceTh2 CellsCell Line TumorNLR Family Pyrin Domain-Containing 3 ProteinImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPromoter Regions GeneticInterleukin 3Oligonucleotide Array Sequence AnalysisMice KnockoutCD40integumentary systemReverse Transcriptase Polymerase Chain ReactionZAP70Gene Expression ProfilingCell DifferentiationNeoplasms ExperimentalAsthmaCell biologyGene Expression Regulation NeoplasticMice Inbred C57BLInterleukin 10Interferon Regulatory FactorsInterleukin 12biology.proteinNIH 3T3 CellsTrans-ActivatorsFemaleInterleukin-4Carrier ProteinsProtein BindingSignal TransductionNature immunology
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Nitric oxide enhances Th9 cell differentiation and airway inflammation

2014

International audience; Th9 cells protect hosts against helminthic infection but also mediate allergic disease. Here we show that nitric oxide (NO) promotes Th9 cell polarization of murine and human CD4(+) T cells. NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2. NO also increases p53-mediated IL-2 production, STAT5 phosphorylation and IRF4 expression, all essential for Th9 polarization. NO also increases the expression of TGFβR and IL-4R, pivotal to Th9 polarization. OVA-sensitized mice treated with an NO donor developed more severe airway inflammation. Transferred Th9 cells induced airway inflammation, which was exacerbated by NO and blocked by anti-IL-9 antibody.…

CD4-Positive T-LymphocytesInterleukin 2[SDV]Life Sciences [q-bio]Cellular differentiationNitric Oxide Synthase Type IIGeneral Physics and AstronomyMice TransgenicInflammationCell SeparationNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyNitric oxideMicechemistry.chemical_compoundEosinophiliaSTAT5 Transcription FactormedicineAnimalsHumansInterleukin 9Cells CulturedInflammationMice Inbred BALB CMultidisciplinarybiologyNitrosylationInterleukin-9Cell DifferentiationGeneral Chemistryrespiratory systemFlow Cytometry3. Good healthCell biologyMice Inbred C57BLchemistryInterferon Regulatory FactorsImmunologyLeukocytes Mononuclearbiology.proteinInterleukin-2Mdm2Tumor Suppressor Protein p53medicine.symptomAntibodymedicine.drugNature Communications
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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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Glycoprotein 96-activated dendritic cells induce a CD8-biased T cell response.

2005

Heat shock proteins (Hsps) are able to induce protective immune responses against pathogens and tumors after injection into immunocompetent hosts. The activation of components of the adaptive immune system, including cytotoxic T lymphocytes specific for pathogen- or tumor-derived peptides, is crucial for the establishment of immuno- protection. Hsps acquire these peptides during intracellular protein degradation and when released during necrotic cell death, facilitate their uptake and Minor Histocompatibility Complex (MHC)-restricted representation by professional antigen-presenting cells (APCs). In addition, the interaction of Hsps with APCs, including the Endoplasmatic Reticulum (ER)-resi…

CD4-Positive T-LymphocytesLipopolysaccharidesAntigen-Presenting CellsBone Marrow CellsMice TransgenicReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexLymphocyte ActivationBiochemistryMiceImmune systemHeat shock proteinCytotoxic T cellAnimalsHumansAntigen-presenting cellCells CulturedMembrane GlycoproteinsToll-Like ReceptorsCell DifferentiationCell BiologyDendritic cellDendritic CellsOriginal ArticlesAcquired immune systemLymphocyte SubsetsCell biologyMice Inbred C57BLToll-Like Receptor 4biology.proteinInflammation MediatorsCD8Signal TransductionCell stresschaperones
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Co-development of naive CD4+ cells towards T helper Type 1 or T helper type 2 cells induced by a combination of IL.-12 and IL-4

1997

Abstract Cytokines were found to play a key role in Th cell differentiation. Among them IL-12 was shown to be a potent differentiation factor for Th1 cells, whereas IL-4 is the only known cytokine that promotes the development of Th2 cells. Upon addition of comparable amounts of IL-4 and IL-12 to a primary culture of naive CD4 + T cells activated by immobilized anti-CD3 mAb, it was found that the Th1-inducing capacity of IL-12 is dominated by the Th2-promoting effect of IL-4. However, high amounts of IL-12 (10,000 U/ml) in combination with low amounts of IL-4 (100 U/ml) led to the development of a Th cell population that, upon rechallenge, showed a substantial secondary IFN-γ (Th1 cytokine)…

CD4-Positive T-LymphocytesMaleCellular differentiationmedicine.medical_treatmentImmunologyInterferon-gammaMiceInterleukin 21Th2 CellsmedicineAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorCells CulturedInterleukin 4Mice Inbred BALB CCD40biologyCell DifferentiationHematologyTh1 CellsInterleukin-12Molecular biologyDrug CombinationsCytokineMice Inbred DBAImmunologyMice Inbred CBAInterleukin 12biology.proteinFemaleInterleukin-4Immunobiology
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Deficiency in the Transcription Factor Interferon Regulatory Factor (Irf)-2 Leads to Severely Compromised Development of Natural Killer and T Helper …

2000

Interferon (IFN) regulatory factor (IRF)-2 was originally described as an antagonist of IRF-1–mediated transcriptional regulation of IFN-inducible genes. IRF-1−/− mice exhibit defective T helper type 1 (Th1) cell differentiation. We have used experimental leishmaniasis to show that, like IRF-1−/− mice, IRF-2−/− mice are susceptible to Leishmania major infection due to a defect in Th1 differentiation. Natural killer (NK) cell development is compromised in both IRF-1−/− and IRF-2−/− mice, but the underlying mechanism differs. NK (but not NK+ T) cell numbers are decreased in IRF-2−/− mice, and the NK cells that are present are immature in phenotype. Therefore, like IRF-1, IRF-2 is required for…

CD4-Positive T-LymphocytesMaleInterferon Regulatory Factor 2Cellular differentiationImmunologyLeishmaniasis CutaneousBiologyNitric OxideTh1MiceInterleukin 21Immune systemBone MarrowInterferonmedicineAnimalsImmunology and AllergyLymphocyte CountLeishmania majorInterleukin-15Mice KnockoutLeishmaniaMice Inbred BALB Cnatural killer cellsCell DifferentiationTh1 CellsInterleukin-12Cell biologyDNA-Binding ProteinsKiller Cells NaturalMice Inbred C57BLRepressor ProteinsDisease Models AnimalInterleukin 15interferon regulatory factorImmunologyInterleukin 12FemaleOriginal ArticleDisease SusceptibilityInterferon Regulatory Factor-2interleukin 15Transcription FactorsInterferon regulatory factorsmedicine.drugJournal of Experimental Medicine
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Antibodies against tumor necrosis factor (TNF) induce T-cell apoptosis in patients with inflammatory bowel diseases via TNF receptor 2 and intestinal…

2011

Background & Aims The anti–tumor necrosis factor (TNF) antibodies infliximab, adalimumab, and certolizumab pegol have proven clinical efficacy in Crohn's disease. Here, we assessed the effects of anti-TNF antibodies on apoptosis in inflammatory bowel disease (IBD). Methods CD14 + macrophages and CD4 + T cells were isolated from peripheral blood and lamina propria mononuclear cells from patients with IBD and control patients. Cell surface markers and apoptosis were assessed by immunohistology and fluorescence-activated cell sorting techniques. Results Lamina propria CD14 + macrophages showed significantly more frequent and higher membrane-bound TNF (mTNF) expression than CD4 + T cells in IBD…

CD4-Positive T-LymphocytesMaleNecrosisCD14Anti-Inflammatory AgentsLipopolysaccharide ReceptorsApoptosisEnzyme-Linked Immunosorbent AssayBiologyAntibodies Monoclonal HumanizedReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellPolyethylene GlycolsImmunoglobulin Fab FragmentsYoung AdultmedicineHumansReceptors Tumor Necrosis Factor Type IIAntigen-presenting cellAgedLamina propriaHepatologyCluster of differentiationTumor Necrosis Factor-alphaMacrophagesGastroenterologyAdalimumabAntibodies MonoclonalMiddle AgedFlow CytometryInflammatory Bowel DiseasesInfliximabmedicine.anatomical_structureApoptosisCase-Control StudiesImmunologyCertolizumab PegolTumor necrosis factor alphaFemalemedicine.symptomGastroenterology
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