Search results for "Interferon Regulatory Factors"

showing 10 items of 26 documents

Reciprocal regulation of the Il9 locus by counteracting activities of transcription factors IRF1 and IRF4.

2017

The T helper 9 (Th9) cell transcriptional network is formed by an equilibrium of signals induced by cytokines and antigen presentation. Here we show that, within this network, two interferon regulatory factors (IRF), IRF1 and IRF4, display opposing effects on Th9 differentiation. IRF4 dose-dependently promotes, whereas IRF1 inhibits, IL-9 production. Likewise, IRF1 inhibits IL-9 production by human Th9 cells. IRF1 counteracts IRF4-driven Il9 promoter activity, and IRF1 and IRF4 have opposing function on activating histone modifications, thus modulating RNA polymerase II recruitment. IRF1 occupancy correlates with decreased IRF4 abundance, suggesting an IRF1-IRF4-binding competition at the I…

0301 basic medicineCD4-Positive T-LymphocytesScienceCellular differentiationAntigen presentationGeneral Physics and AstronomyRNA polymerase IIMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciences0302 clinical medicineInterferonmedicineAnimalsHumansInterleukin 9Transcription factorMice KnockoutMultidisciplinaryGene Expression ProfilingQInterleukin-9Cell DifferentiationGeneral ChemistryT-Lymphocytes Helper-InducerCell biologyMice Inbred C57BL030104 developmental biologyIRF1Interferon Regulatory Factorsbiology.protein030215 immunologyInterferon regulatory factorsmedicine.drugInterferon Regulatory Factor-1Nature communications
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TGF-β inhibitor Smad7 regulates dendritic cell-induced autoimmunity

2017

TGF-β is an anti-inflammatory cytokine whose signaling is negatively controlled by Smad7. Previously, we established a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in dendritic cells (DCs) remains elusive. Here, we demonstrate that DC-specific Smad7 deficiency resulted in elevated expression of the transcription factors Batf3 and IRF8, leading to increased frequencies of CD8(+)CD103(+) DCs in the spleen. Furthermore, Smad7-deficient DCs expressed higher levels of indoleamine 2,3-dioxygenase (IDO), an enzyme associated with tolerance induction. Mice devoid of Smad7 specifically in DCs are resistant to the development of experimental autoimmune ence…

0301 basic medicineEncephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentCellular differentiationAutoimmunitychemical and pharmacologic phenomenaCD8-Positive T-LymphocytesBiologyT-Lymphocytes RegulatorySmad7 ProteinImmune toleranceMice03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaImmune TolerancemedicineAnimalsIndoleamine-Pyrrole 23-DioxygenaseMultidisciplinaryintegumentary systemExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsDendritic CellsDendritic cellTransforming growth factor betamedicine.diseaseCell biologyMice Inbred C57BLTolerance inductionBasic-Leucine Zipper Transcription Factors030104 developmental biologyCytokinePNAS PlusInterferon Regulatory FactorsImmunologybiology.proteinCytokinesSpleenCD8Signal Transduction030215 immunology
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Single-cell trajectories reconstruction, exploration and mapping of omics data with STREAM

2019

Single-cell transcriptomic assays have enabled the de novo reconstruction of lineage differentiation trajectories, along with the characterization of cellular heterogeneity and state transitions. Several methods have been developed for reconstructing developmental trajectories from single-cell transcriptomic data, but efforts on analyzing single-cell epigenomic data and on trajectory visualization remain limited. Here we present STREAM, an interactive pipeline capable of disentangling and visualizing complex branching trajectories from both single-cell transcriptomic and epigenomic data. We have tested STREAM on several synthetic and real datasets generated with different single-cell techno…

0301 basic medicineEpigenomicsMultifactor Dimensionality ReductionComputer scienceGeneral Physics and Astronomy02 engineering and technologyOmics dataMyoblastsMiceSingle-cell analysisGATA1 Transcription FactorMyeloid CellsLymphocyteslcsh:ScienceData processingMultidisciplinaryQGene Expression Regulation DevelopmentalRNA sequencingCell DifferentiationGenomics021001 nanoscience & nanotechnologyData processingDNA-Binding ProteinsInterferon Regulatory FactorsSingle-Cell Analysis0210 nano-technologyAlgorithmsOmics technologiesSignal TransductionLineage differentiationScienceComputational biologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesErythroid CellsAnimalsCell LineageGeneral Chemistrydevelopmental trajectories visualizationHematopoietic Stem CellsPipeline (software)Visualization030104 developmental biologyTheoryofComputation_MATHEMATICALLOGICANDFORMALLANGUAGESCellular heterogeneitySingle cell analysilcsh:QGene expressionTranscriptomeTranscription FactorsNature Communications
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Meta-analysis identifies novel risk loci and yields systematic insights into the biology of male-pattern baldness

2017

Male-pattern baldness (MPB) is a common and highly heritable trait characterized by androgen-dependent, progressive hair loss from the scalp. Here, we carry out the largest GWAS meta-analysis of MPB to date, comprising 10,846 early-onset cases and 11,672 controls from eight independent cohorts. We identify 63 MPB-associated loci (P<5 × 10−8, METAL) of which 23 have not been reported previously. The 63 loci explain ∼39% of the phenotypic variance in MPB and highlight several plausible candidate genes (FGF5, IRF4, DKK2) and pathways (melatonin signalling, adipogenesis) that are likely to be implicated in the key-pathophysiological features of MPB and may represent promising targets for the de…

0301 basic medicineMaleCandidate genegenetics [Trans-Activators]SRD5A2 protein humanMedizinGeneral Physics and Astronomygenetics [3-Oxo-5-alpha-Steroid 4-Dehydrogenase]Genome-wide association studyBioinformatics0302 clinical medicinegenetics [Interferon Regulatory Factors]GenotypeMelatoninGeneticsMultidisciplinaryAdipogenesisEBF1 protein humanintegumentary systemgenetics [Intercellular Signaling Peptides and Proteins]QPhenotypeFGF5 protein humangenetics [Membrane Proteins]Phenotype030220 oncology & carcinogenesisMeta-analysisUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]Interferon Regulatory FactorsIntercellular Signaling Peptides and ProteinsMale-pattern baldnessddc:500Signal TransductionDKK2 protein humanGenotypeFibroblast Growth Factor 53-Oxo-5-alpha-Steroid 4-Dehydrogenase/genetics; Adipogenesis/genetics; Alopecia/genetics; Case-Control Studies; Fibroblast Growth Factor 5/genetics; Genetic Association Studies; Genome-Wide Association Study; Genotype; Humans; Intercellular Signaling Peptides and Proteins/genetics; Interferon Regulatory Factors/genetics; Male; Melatonin; Membrane Proteins/genetics; Phenotype; Signal Transduction/genetics; Trans-Activators/geneticsScienceGenomicsBiologygenetics [Signal Transduction]General Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesinterferon regulatory factor-43-Oxo-5-alpha-Steroid 4-DehydrogenasemedicineHumansgenetics [Adipogenesis]Genetic Association Studiesgenetics [Alopecia]Case-control studyMembrane ProteinsAlopeciaGeneral Chemistrymedicine.diseasegenetics [Fibroblast Growth Factor 5]030104 developmental biologyCase-Control StudiesTrans-ActivatorsGenome-Wide Association Study
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IRF8 Transcription Factor Controls Survival and Function of Terminally Differentiated Conventional and Plasmacytoid Dendritic Cells, Respectively

2016

International audience; Interferon regulatory factor-8 (IRF8) has been proposed to be essential for development of monocytes, plasmacytoid dendritic cells (pDCs) and type 1 conventional dendritic cells (cDC1s) and remains highly expressed in differentiated DCs. Transcription factors that are required to maintain the identity of terminally differentiated cells are designated `' terminal selectors.'' Using BM chimeras, conditional Irf8(fl/fl) mice and various promotors to target Cre recombinase to different stages of monocyte and DC development, we have identified IRF8 as a terminal selector of the cDC1 lineage controlling survival. In monocytes, IRF8 was necessary during early but not late d…

0301 basic medicineT-LymphocytesCellular differentiationImmunologyCre recombinasePlasmacytoid dendritic cellBiologyMonocytesMice03 medical and health sciences0302 clinical medicineInterferonmedicineAnimalsImmunology and AllergyPromoter Regions GeneticMonocyteCell DifferentiationDendritic CellsDendritic cellCell biologyMice Inbred C57BL030104 developmental biologyInfectious Diseasesmedicine.anatomical_structureInterferon Regulatory FactorsInterferon Type ICancer research[SDV.IMM]Life Sciences [q-bio]/ImmunologyIRF8Transcription Factors030215 immunologyIRF4medicine.drugImmunity
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The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6

2008

The proinflammatory cytokine IL-6 seems to have an important role in the intestinal inflammation that characterizes inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis. However, little is known about the molecular mechanisms regulating IL-6 production in IBD. Here, we assessed the role of the transcriptional regulator IFN regulatory factor-4 (IRF4) in this process. Patients with either Crohn disease or ulcerative colitis exhibited increased IRF4 expression in lamina propria CD3+ T cells as compared with control patients. Consistent with IRF4 having a regulatory function in T cells, in a mouse model of IBD whereby colitis is induced in RAG-deficient mice by transp…

AdultCD4-Positive T-LymphocytesMaleAdoptive cell transferRecombinant Fusion ProteinsT-LymphocytesCD3T cellAdoptive Transfer; Adult; Animals; Apoptosis; CD4-Positive T-Lymphocytes; Colitis; Cytokines; DNA-Binding Proteins; Female; Gene Expression Regulation; Humans; Inflammatory Bowel Diseases; Interferon Regulatory Factors; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice Inbred C57BL; Mice Knockout; Middle Aged; Oxazolone; Receptors Interleukin-6; Recombinant Fusion Proteins; T-Lymphocytes; Trinitrobenzenesulfonic AcidApoptosisProinflammatory cytokineMiceIntestinal mucosamedicineAnimalsHumansIntestinal MucosaColitisInterleukin 6Mice KnockoutbiologyInterleukin-6OxazoloneGeneral MedicineMiddle AgedColitisInflammatory Bowel Diseasesmedicine.diseaseAdoptive TransferReceptors Interleukin-6Ulcerative colitisDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationTrinitrobenzenesulfonic AcidInterferon Regulatory FactorsImmunologybiology.proteinCytokinesFemaleResearch ArticleJournal of Clinical Investigation
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IRF4 regulates IL-17A promoter activity and controls RORγt-dependent Th17 colitis in vivo

2011

The transcription factor IRF4 is involved in several T-cell-dependent chronic inflammatory diseases. To elucidate the mechanisms for pathological cytokine production in colitis, we addressed the role of the IRF transcription factors in human inflammatory bowel disease (IBD) and experimental colitis.IRF levels and cytokine production in IBD patients were studied as well as the effects of IRF4 deficiency in experimental colitis.In contrast to IRF1, IRF5, and IRF8, IRF4 expression in IBD was augmented in the presence of active inflammation. Furthermore, IRF4 levels significantly correlated with IL-6 and IL-17 mRNA expression and to a lesser extent with IL-22 mRNA expression in IBD. To further …

AdultMaleElectrophoretic Mobility Shift AssayInflammatory bowel diseasePolymerase Chain Reaction03 medical and health sciencesMice0302 clinical medicineCrohn DiseaseRAR-related orphan receptor gammaImmunology and AllergyMedicineAnimalsHumansColitisInterleukin 6Promoter Regions GeneticTranscription factor030304 developmental biology0303 health sciencesCrohn's diseasebiologybusiness.industryInterleukin-6Interleukin-17GastroenterologyMiddle AgedNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseColitisInflammatory Bowel Diseasesdigestive system diseases3. Good health030220 oncology & carcinogenesisImmunologyInterferon Regulatory Factorsbiology.proteinTh17 CellsColitis UlcerativeFemaleInterleukin 17businessInterferon regulatory factors
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IL-27 improves migrational and antiviral potential of CB dendritic cells.

2013

Abstract Interleukin (IL)-27 is known to be increased considerably in cord blood (CB) dendritic cells (DCs) after TLR ligation. Previously, we demonstrated that also basal IL-27 levels are higher in CB DCs. Here, we examined effects of IL-27 on monocyte derived dendritic cells (moDCs) to approach its particular role in the specialized immune system of the human neonate. Exogenous IL-27 promotes IL-27 transcription in CB and adult blood (AB) moDCs. IL-27 acts on CB moDCs primarily by significantly augmenting IL-27 protein, secondarily by increasing transcription of CXCL10 among other chemokines, chemokine receptor CCR1, interferon stimulated genes, transcription factor IRF8 and genes involve…

CCR1AdultChemokineTranscription GeneticImmunologyAntigen presentationReceptors CCR1MonocytesChemokine receptorInterferonCell MovementmedicineImmunology and AllergyCXCL10HumansCells CulturedbiologyTumor Necrosis Factor-alphaInterleukinsInterleukin-8Infant NewbornInterleukinCell DifferentiationGeneral MedicineDendritic CellsFetal BloodChemokine CXCL10STAT1 Transcription FactorGene Expression RegulationInterferon Regulatory Factorsbiology.proteinCancer researchIRF8medicine.drugSignal TransductionHuman 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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