Search results for "DNA-BINDING PROTEIN"

showing 10 items of 449 documents

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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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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Differential Regulatory Capacity of CD25+ T Regulatory Cells and Preactivated CD25+ T Regulatory Cells on Development, Functional Activation, and Pro…

2004

Abstract CD25+ T regulatory (Treg) cells play a central role regarding the maintenance of peripheral tolerance via suppression of autoaggressive CD4+ T cells, CD8+ T cells, and Th1 cells. In this study we demonstrate that CD25+ Treg cells can also suppress the differentiation of murine conventional CD4+ T cells toward Th2 cells in a contact-dependent manner. However, the cytokine production and proliferation of established Th2 cells could not be inhibited by freshly isolated CD25+ Treg cells, whereas a strong inhibition of differentiated Th2 cells by in vitro preactivated CD25+ Treg cells could be observed. Inhibition of both conventional CD4+ T cells and Th2 cells is accompanied by a stron…

CD4-Positive T-LymphocytesImmunologySuccinimideschemical and pharmacologic phenomenaLymphocyte ActivationMiceInterleukin 21Th2 CellsT-Lymphocyte SubsetsAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellInterleukin 3Mice Inbred BALB CCD40biologyPeripheral toleranceForkhead Transcription FactorsReceptors Interleukin-2hemic and immune systemsFluoresceinsCell biologyDNA-Binding ProteinsMice Inbred C57BLbiology.proteinInterleukin 12CytokinesThe Journal of Immunology
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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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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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A new model of chronic colitis in SCID mice induced by adoptive transfer of CD62L+ CD4+ T cells: insights into the regulatory role of interleukin-6 o…

2003

<i>Objective:</i> The proinflammatory cytokine interleukin (IL)-6 is involved in various chronic inflammatory processes. IL-6 is a predominant cytokine produced by lamina propria T cells in Crohn’s disease and experimental colitis. This study was designed to examine the effect of a neutralizing IL-6-receptor (IL-6R) antibody on the programmed cell death of mucosal T cells in the CD62L+ CD4+ SCID transfer model of chronic experimental colitis in mice and to gain more insight into the pathogenesis of this transfer colitis model. <i>Methods:</i> For adoptive transfer, we isolated CD62L+ CD4+ double-positive T cells from wild-type BALB/c mice followed by intraperitoneal …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorAdoptive cell transferCell TransplantationColonApoptosisMice SCIDPathology and Forensic MedicineProinflammatory cytokineInterleukin 21MiceInterleukin 25In Situ Nick-End LabelingAnimalsIL-2 receptorIntestinal MucosaL-SelectinInterleukin 6Antibodies BlockingMolecular BiologyMice Inbred BALB CbiologyInterleukin-6InterleukinCell BiologyGeneral MedicineFlow CytometryAdoptive TransferReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalImmunologybiology.proteinTrans-ActivatorsInterleukin 18Colitis UlcerativeSevere Combined ImmunodeficiencySpleenPathobiology : journal of immunopathology, molecular and cellular biology
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Activation pattern of signal transducers and activators of transcription (STAT) factors in inflammatory bowel diseases.

2005

Cytokine signaling pathways involving transcription factors of the signal transducers and activators of transcription (STAT) family play a key role in the pathogenesis of inflammatory bowel diseases (IBD). STAT proteins are latent cytoplasmic transcription factors that induce transcription upon phosphorylation, dimerization, and nuclear translocation. However, their activation pattern in IBD is poorly understood. The aim of our study was to characterize STAT-expression in IBD.Mononuclear cells were isolated from 36 colonic specimens of Crohn's disease, ulcerative colitis, or from control patients. Cells were stimulated overnight with antibodies against human CD2 and CD28 and mononuclear cel…

CD4-Positive T-LymphocytesSTAT3 Transcription FactorColonActivation patternstatTranscription (biology)MedicineHumansSTAT4Transcription factorHepatologybusiness.industryActivator (genetics)digestive oral and skin physiologyGastroenterologySTAT2 Transcription FactorSTAT3 Transcription FactorSTAT4 Transcription FactorInflammatory Bowel Diseasesdigestive system diseasesDNA-Binding ProteinsSTAT1 Transcription FactorCase-Control StudiesImmunologyCancer researchTrans-ActivatorsSignal transductionbusinessSTAT6 Transcription FactorThe American journal of gastroenterology
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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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X Chromosome Contribution to the Genetic Architecture of Primary Biliary Cholangitis

2021

Background & aims: Genome-wide association studies in primary biliary cholangitis (PBC) have failed to find X chromosome (chrX) variants associated with the disease. Here, we specifically explore the chrX contribution to PBC, a sexually dimorphic complex autoimmune disease. Methods: We performed a chrX-wide association study, including genotype data from 5 genome-wide association studies (from Italy, United Kingdom, Canada, China, and Japan; 5244 case patients and 11,875 control individuals). Results: Single-marker association analyses found approximately 100 loci displaying P < 5 × 10-4, with the most significant being a signal within the OTUD5 gene (rs3027490; P = 4.80 × 10-6; odds…

Canadian-US PBC Consortium0301 basic medicineMaleLinkage disequilibriumGenome-wide association studyDiseasePBCSettore MED/03 - GENETICA MEDICALinkage Disequilibrium0302 clinical medicineUK-PBC ConsortiumGenotypeMitochondrial Precursor Protein Import Complex ProteinsItalian PBC Genetics Study GroupOdds RatioX-Wide Association StudyJapan PBC-GWAS ConsortiumX chromosomeGeneticsLiver Cirrhosis BiliaryGastroenterologyForkhead Transcription FactorsDNA-Binding ProteinsShal Potassium Channels030211 gastroenterology & hepatologyFemaleAdultMonosaccharide Transport ProteinsSuperenhancerLocus (genetics)Single-nucleotide polymorphismBiologyProtein Serine-Threonine KinasesPolymorphism Single NucleotideArticleWhite People03 medical and health sciencesAsian PeopleProto-Oncogene ProteinsEndopeptidasesHumansCell LineageGenetic Predisposition to DiseaseMeta-analysiGenetic associationChromosomes Human XGastroenterology & HepatologyHepatology1103 Clinical SciencesMeta-analysis030104 developmental biologyGenetic Loci1114 Paediatrics and Reproductive MedicineMeta-analysis; Superenhancer; X-Wide Association Study1109 NeurosciencesCarrier ProteinsGenome-Wide Association Study
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The role of hypoxia-induced factors in tumor progression.

2004

Abstract Learning Objectives After completing this course, the reader will be able to: Describe hypoxia-induced mechanisms for cell survival. Discuss hypoxia-induced gene expression. Relate hypoxia and glucose metabolism. Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit atCME.TheOncologist.com Hypoxia is a common characteristic of locally advanced solid tumors that has been associated with diminished therapeutic response and, more recently, with malignant progression, that is, an increasing probability of recurrence, locoregional spread, and distant metastasis. Emerging evidence indicates that the effect of hypoxia on malignant progression is mediated by a…

Cancer ResearchAngiogenesisCell SurvivalRegulatorBiologyNeoplasmsmedicineHumansNuclear proteinSelection GeneticTranscription factorG alpha subunitRegulation of gene expressionHelix-Loop-Helix MotifsNuclear ProteinsHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaDNA-Binding ProteinsGene Expression Regulation NeoplasticCell Transformation NeoplasticGlucoseOncologyTumor progressionImmunologyCancer researchDisease ProgressionHypoxia-Inducible Factor 1medicine.symptomTranscription FactorsThe oncologist
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