Search results for "MESH: Promoter Regions"

showing 3 items of 3 documents

Stat3 and Gfi-1 Transcription Factors Control Th17 Cell Immunosuppressive Activity via the Regulation of Ectonucleotidase Expression

2012

International audience; Although Th17 cells are known to promote tissue inflammation and autoimmunity, their role during cancer progression remains elusive. Here, we showed that in vitro Th17 cells generated with the cytokines IL-6 and TGF-β expressed CD39 and CD73 ectonucleotidases, leading to adenosine release and the subsequent suppression of CD4(+) and CD8(+) T cell effector functions. The IL-6-mediated activation of the transcription factor Stat3 and the TGF-β-driven downregulation of Gfi-1 transcription factor were both essential for the expression of ectonucleotidases during Th17 cell differentiation. Stat3 supported whereas Gfi-1 repressed CD39 and CD73 expression by binding to thei…

Adoptive cell transferMESH : Transcription FactorsCellular differentiationMESH: Th17 CellsT-LymphocytesCellMESH : Promoter Regions GeneticMESH : RNA Small InterferingMESH: Mice KnockoutMice0302 clinical medicineTransforming Growth Factor betaMESH: RNA Small InterferingMESH : STAT3 Transcription FactorImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyEctonucleotidaseMESH: AnimalsRNA Small InterferingSTAT3MESH: Lymphocytes Tumor-InfiltratingPromoter Regions GeneticMESH: Antigens CD5'-NucleotidaseRegulation of gene expressionMice Knockout0303 health sciencesMESH : Gene Expression RegulationApyraseMESH: STAT3 Transcription FactorMESH: Transcription FactorsMESH: Gene Expression RegulationMESH : Mice TransgenicCell biologyMESH : Lymphocytes Tumor-InfiltratingDNA-Binding ProteinsMESH : ApyraseInfectious Diseasesmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : DNA-Binding ProteinsMESH: ApyraseSTAT3 Transcription Factor[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Interleukin-6MESH: Mice TransgenicT cellImmunologyMice TransgenicMESH : Mice Inbred C57BLBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingMESH: Mice Inbred C57BLAntigens CDMESH: Promoter Regions GeneticMESH : 5'-NucleotidaseMESH : MicemedicineMESH : Antigens CDMESH : Th17 CellsAnimalsTranscription factorMESH: MiceMESH: Transforming Growth Factor beta030304 developmental biologyMESH : T-LymphocytesBinding SitesInterleukin-6MESH: Interleukin-6Mice Inbred C57BLMESH: T-LymphocytesMESH : Transforming Growth Factor betaMESH: Binding SitesGene Expression Regulationbiology.proteinMESH : Mice KnockoutTh17 CellsMESH : AnimalsMESH: 5'-NucleotidaseMESH: DNA-Binding ProteinsMESH : Binding Sites030215 immunologyTranscription FactorsImmunity
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The nuclear receptor PPARγ selectively inhibits Th17 differentiation in a T cell–intrinsic fashion and suppresses CNS autoimmunity

2009

T helper cells secreting interleukin (IL)-17 (Th17 cells) play a crucial role in autoimmune diseases like multiple sclerosis (MS). Th17 differentiation, which is induced by a combination of transforming growth factor (TGF)-beta/IL-6 or IL-21, requires expression of the transcription factor retinoic acid receptor-related orphan receptor gamma t (ROR gamma t). We identify the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR gamma) as a key negative regulator of human and mouse Th17 differentiation. PPAR gamma activation in CD4(+) T cells selectively suppressed Th17 differentiation, but not differentiation into Th1, Th2, or regulatory T cells. Control of Th17 differentia…

MESH: Nuclear Receptor Subfamily 1 Group F Member 3Helper-InducerReceptors Retinoic AcidT-LymphocytesMESH: Interleukin-17Cellular differentiationRetinoic AcidPeroxisome proliferator-activated receptorNeurodegenerativeInbred C57BLMedical and Health SciencesMiceInterleukin 210302 clinical medicineGroup FRAR-related orphan receptor gammaMESH: Nuclear Receptor Co-Repressor 2Receptors2.1 Biological and endogenous factorsThyroid HormoneImmunology and AllergyMESH: AnimalsAetiologyEncephalomyelitisPromoter Regions Geneticchemistry.chemical_classificationOrphan receptor0303 health sciencesReceptors Thyroid HormoneInterleukin-17Cell DifferentiationT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 33. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureMESH: Repressor Proteins[SDV.IMM]Life Sciences [q-bio]/ImmunologyInterleukin 17MESH: Cell Differentiationmedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisNuclear Receptor Subfamily 1Member 31.1 Normal biological development and functioningT cellImmunologyBiologyAutoimmune DiseasePromoter RegionsExperimental03 medical and health sciencesGeneticUnderpinning researchMESH: Mice Inbred C57BLInternal medicineMESH: Promoter Regions GeneticGeneticsmedicineAnimalsHumansNuclear Receptor Co-Repressor 2MESH: Receptors Thyroid HormoneMESH: T-Lymphocytes Helper-InducerMESH: Encephalomyelitis Autoimmune ExperimentalMESH: Mice030304 developmental biologyMESH: Receptors Retinoic AcidMESH: HumansInflammatory and immune systemNeurosciencesBrief Definitive ReportCorrectionMESH: Multiple SclerosisBrain DisordersMice Inbred C57BLPPAR gammaRepressor ProteinsEndocrinologyMESH: PPAR gammaNuclear receptorchemistryMESH: DNA-Binding Proteins030217 neurology & neurosurgeryAutoimmuneJournal of Experimental Medicine
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Analysis of RET promoter CpG island methylation using methylation-specific PCR (MSP), pyrosequencing, and methylation-sensitive high-resolution melti…

2016

Background Already since the 1990s, promoter CpG island methylation markers have been considered promising diagnostic, prognostic, and predictive cancer biomarkers. However, so far, only a limited number of DNA methylation markers have been introduced into clinical practice. One reason why the vast majority of methylation markers do not translate into clinical applications is lack of independent validation of methylation markers, often caused by differences in methylation analysis techniques. We recently described RET promoter CpG island methylation as a potential prognostic marker in stage II colorectal cancer (CRC) patients of two independent series. Methods In the current study, we analy…

Male0301 basic medicineMESH: Sequence Analysis DNABisulfite sequencingAnalytic sensitivityMS-HRMMESH : AgedMESH : Promoter Regions GeneticPolymerase Chain Reaction[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineMESH: DNA MethylationMESH : FemaleMESH : Proto-Oncogene Proteins c-retPromoter Regions GeneticMESH: CpG IslandsMESH : Polymerase Chain ReactionGenetics (clinical)MESH: AgedDNA methylationMESH : PrognosisMethylationMESH : CpG IslandsPrognosispyrosequencing030220 oncology & carcinogenesisMESH: Survival AnalysisDNA methylationFemaleMESH : Colorectal NeoplasmsMESH : Sensitivity and SpecificityColorectal NeoplasmsMESH : Male[SDV.CAN]Life Sciences [q-bio]/CancerBiologySensitivity and SpecificityMESH: Proto-Oncogene Proteins c-retHigh Resolution MeltMESH: Prognosis03 medical and health sciencesMESH: Promoter Regions GeneticGeneticsHumansMolecular BiologyAgedMESH: HumansResearchMSPProto-Oncogene Proteins c-retMESH : HumansMESH: Polymerase Chain ReactionSequence Analysis DNASurvival AnalysisMolecular biologyMESH: Sensitivity and SpecificityMESH: Male030104 developmental biologyPyrosequencingIllumina Methylation AssayCpG IslandsCancer biomarkersClinical sensitivityPrimer (molecular biology)MESH : Survival AnalysisRETMESH: FemaleMESH : DNA MethylationMESH: Colorectal NeoplasmsDevelopmental BiologyMESH : Sequence Analysis DNA
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