Search results for "Smad7"

showing 10 items of 12 documents

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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Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis

2018

Background & Aims The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice. Methods We performed immunohistochemical analyses of colon tissues from patients with untreated CD and patients without inflammatory bowel diseases (controls). We obtained mice that expressed splice forms of CYLD (sCYLD mice) without or with SMAD7 (sCYLD/SMAD7 mice) from tr…

0301 basic medicineTranscription FactorBiopsyInbred C57BLTransgenicImmune RegulationSettore MED/12MiceRandom Allocation0302 clinical medicineCrohn DiseaseReference ValuesNeedleIntestinal Mucosaintegumentary systemChemistryBiopsy NeedleGastroenterologyT helper cellFlow CytometryPost-translational ModificationImmunohistochemistryDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structure030211 gastroenterology & hepatologyTumor necrosis factor alphaSignal TransductionGenetically modified mouseRegulatory T cellTransgeneMice TransgenicSmad7 ProteinTransforming Growth Factor beta103 medical and health sciencesImmune systemmedicineAnimalsHumansCytokine SignalingHepatologyAnimalHEK 293 cellsUbiquitinationMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyDisease ModelsCytokine Signaling; Immune Regulation; Post-translational Modification; Transcription Factor; Biopsy Needle; Crohn Disease; Cysteine Endopeptidases; Deubiquitinating Enzyme CYLD; Disease Models Animal; Flow Cytometry; Immunohistochemistry; Intestinal Mucosa; Mice Inbred C57BL; Mice Transgenic; Random Allocation; Reference Values; Signal Transduction; Smad7 Protein; Transforming Growth Factor beta1; UbiquitinationTransforming growth factorGastroenterology
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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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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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TGF-β superfamily signaling is essential for tooth and hair morphogenesis and differentiation

2007

Members of the transforming growth factor beta (TGF-beta) superfamily of signaling molecules are involved in the regulation of many developmental processes that involve the interaction between mesenchymal and epithelial tissues. Smad7 is a potent inhibitor of many members of the TGF-beta family, notably TGF-beta and activin. In this study, we show that embryonic overexpression of Smad7 in stratified epithelia using a keratin 5 promoter, results in severe morphogenetic defects in skin and teeth and leads to embryonic and perinatal lethality. To further analyze the functions of Smad7 in epithelial tissues of adult mice, we used an expression system that allowed a controlled overexpression of …

Cell signalingmedicine.medical_specialtyHistologyMorphogenesisEmbryonic DevelopmentMice TransgenicNerve Tissue ProteinsBiologySmad7 ProteinPathology and Forensic MedicineNestinMice03 medical and health sciences0302 clinical medicineIntermediate Filament ProteinsGenes ReporterTransforming Growth Factor betaInternal medicineMorphogenesismedicineAnimalsHumansTransgenes030304 developmental biology0303 health sciencesR-SMADIntegrasesintegumentary systemTooth Abnormalities[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCell DifferentiationCell BiologyGeneral MedicineHair follicleSurvival AnalysisCell biologyKeratin 5Endocrinologymedicine.anatomical_structureGene Expression RegulationLac OperonTransforming growth factor beta 3030220 oncology & carcinogenesisRabbitsAmeloblastToothHairSignal TransductionTransforming growth factorEuropean Journal of Cell Biology
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Smad7 in T cells drives T helper 1 responses in multiple sclerosis and experimental autoimmune encephalomyelitis

2010

Autoreactive CD4+ T lymphocytes play a vital role in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. Since the discovery of T helper 17 cells, there is an ongoing debate whether T helper 1, T helper 17 or both subtypes of T lymphocytes are important for the initiation of autoimmune neuroinflammation. We examined peripheral blood CD4+ cells from patients with active and stable relapsing-remitting multiple sclerosis, and used mice with conditional deletion or over-expression of the transforming growth factor-beta inhibitor Smad7, to delineate the role of Smad7 in T cell differentiation and autoimmune neuroinflammation. We found that Smad…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisT helper 1Regulatory T cellT cellMolecular Sequence DataMice TransgenicBiologySmad7 ProteinMiceInterleukin 21medicineAnimalsHumansCytotoxic T cellAmino Acid SequenceIL-2 receptorAntigen-presenting cellMice Knockoutintegumentary systemEAEimmune regulationCD28Original ArticlesTh1 CellsNatural killer T cellMice Inbred C57BLmedicine.anatomical_structureT cell responsesImmunologyNeurology (clinical)Brain
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Hepatocyte-Specific Smad7 Expression Attenuates TGF-β–Mediated Fibrogenesis and Protects Against Liver Damage

2008

Background & Aims The profibrogenic role of transforming growth factor (TGF)-β in liver has mostly been attributed to hepatic stellate cell activation and excess matrix synthesis. Hepatocytes are believed to contribute to increased rates of apoptosis. Methods Primary hepatocyte outgrowths and AML12 cells were used as an in vitro model to detect TGF-β effects on the cellular phenotype and expression profile. Furthermore, a transgenic mouse model was used to determine the outcome of hepatocyte-specific Smad7 expression on fibrogenesis following CCl 4 -dependent damage. Samples from patients with chronic liver diseases were assessed for (partial) epithelial-to-mesenchymal transition (EMT) in h…

Liver CirrhosisMaleTime FactorsCell SurvivalApoptosisMice TransgenicBiologyCell LineSmad7 ProteinMiceTransforming Growth Factor betaFibrosismedicineAnimalsHumansSchistosomiasisEpithelial–mesenchymal transitionCarbon TetrachlorideCells CulturedOligonucleotide Array Sequence AnalysisR-SMADHepatologyGene Expression ProfilingGastroenterologyHepatitis Bmedicine.diseaseHepatic stellate cell activationMice Inbred C57BLCTGFDisease Models AnimalPhenotypemedicine.anatomical_structureHepatocyteCell TransdifferentiationHepatocytesCancer researchHepatic stellate cellCollagenTransforming growth factorGastroenterology
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The Role of Transforming Growth Factor-β1 in Airway Inflammation of Childhood Asthma

2013

TGF-beta-targeting structural and inflammatory cells has been implicated in the mechanisms leading to the inflammatory and restructuring processes in asthma, suggesting an impact of TGF-beta1 signaling on the development and persistency of this disease. We investigated the potential early involvement of TGF-beta1 activity in the immunological and molecular mechanisms underlying progression of inflammation in childhood asthma. We evaluated the levels of TGF-beta1 in induced sputum supernatants (ISSs) and the expression of small mother cell against decapentaplegic (Smad) 2 and Smad7 proteins in induced sputum cells (ISCs) from children with intermittent asthma (IA), moderate asthma (MA) and c…

MaleNeutrophilsSmad2 ProteinSMADEosinophilAdrenal Cortex HormoneSeverity of Illness IndexAdrenal Cortex HormonesImmunology and AllergyAge FactorPhosphorylationChildLungNeutrophilAge FactorsBronchodilator Agentsmedicine.anatomical_structureFemalemedicine.symptomCase-Control StudieHumanSignal TransductionGranulocyte activationAdolescentImmunologyAge Factors; Humans; Child; Macrophage-1 Antigen; Adrenal Cortex Hormones; Granulocytes; Neutrophils; Phosphorylation; Eosinophils; Adolescent; Signal Transduction; Male; Severity of Illness Index; Respiratory Mucosa; Asthma; Transforming Growth Factor beta1; Epithelial Cells; Lung; Smad2 Protein; Case-Control Studies; Smad7 Protein; Sputum; Administration Inhalation; Bronchodilator Agents; Cell Line; Female; Cell AdhesionMacrophage-1 AntigenCD18InflammationRespiratory MucosaGranulocyteCell LineSmad7 ProteinTransforming Growth Factor beta1Administration InhalationCell AdhesionmedicineHumansCell adhesionBronchodilator AgentPharmacologyEpithelial Cellbusiness.industrySputumGranulocyteEpithelial CellsEosinophilAsthmaEosinophilsCase-Control StudiesImmunologySputumbusinessGranulocytesInternational Journal of Immunopathology and Pharmacology
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Docosahexaenoic acid reduces suppressive and migratory functions of CD4CD25 regulatory T-cells

2009

Immunological tolerance is one of the fundamental aspects of the immune system. The CD4(+)CD25(+) regulatory T (Treg) cells have emerged as key players in the development of tolerance to self and foreign antigens. However, little is known about the endogenous factors and mechanisms controlling their suppressive capacity on immune response. In this study, we observed that docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, diminished, in a dose-dependent manner, the capacity of Treg cells to inhibit the CD4(+)CD25(-) effector T-cell proliferation. DHA not only reduced the migration of Treg cells toward chemokines but also downregulated the mRNA expression of CCR-4 and CXCR-4 in Tr…

MaleReceptors CXCR4Chemokineextracellular signal-regulated kinase 1/2Receptors CCR4Docosahexaenoic Acidschemical and pharmacologic phenomenaQD415-436T-Lymphocytes RegulatoryBiochemistryMicehistone desacetylase 7EndocrinologyImmune systemAntigenAntigens CDCell MovementTransforming Growth Factor betaAnimalsCTLA-4 AntigenRNA MessengerIL-2 receptorCells CulturedCell ProliferationDose-Response Relationship DrugbiologySmad7Reverse Transcriptase Polymerase Chain ReactionInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription Factorshemic and immune systemsCell BiologyTransforming growth factor betaInterleukin-10Cell biologyMice Inbred C57BLInterleukin 10Docosahexaenoic acidImmunologybiology.proteinResearch ArticleJournal of Lipid Research
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Mongersen, an oral SMAD7 antisense oligonucleotide, and crohn's disease

2015

Crohn's disease-related inflammation is characterized by reduced activity of the immunosuppressive cytokine transforming growth factor β1 (TGF-β1) due to high levels of SMAD7, an inhibitor of TGF-β1 signaling. Preclinical studies and a phase 1 study have shown that an oral SMAD7 antisense oligonucleotide, mongersen, targets ileal and colonic SMAD7.In a double-blind, placebo-controlled, phase 2 trial, we evaluated the efficacy of mongersen for the treatment of persons with active Crohn's disease. Patients were randomly assigned to receive 10, 40, or 160 mg of mongersen or placebo per day for 2 weeks. The primary outcomes were clinical remission at day 15, defined as a Crohn's Disease Activit…

MaleSMAD7 antisense oligonucleotidemedicine.medical_treatmentOligonucleotidesPharmacologyPLACEBO-CONTROLLED TRIALTHERAPYGastroenterologylaw.inventionACTIVATIONImmunosuppressive AgentGlucocorticoidRandomized controlled trialCrohn DiseaselawOligonucleotideMedicineYoung adultCrohn's diseaseSettore MED/12 - GastroenterologiabiologyINDUCTIONMedicine (all)Remission InductionGeneral MedicineMiddle AgedCrohn's diseaseCytokineC-Reactive ProteinCombinationDrug Therapy CombinationFemaleDrugImmunosuppressive AgentsCOLITISHumanAdultmedicine.medical_specialtyAdolescentINFLAMMATORY-BOWEL-DISEASE PLACEBO-CONTROLLED TRIAL NECROSIS-FACTOR-ALPHA TGF-BETA-1-MEDIATED SUPPRESSION COLITIS INDUCTION ACTIVATION EFFICACY THERAPY MICEPlaceboSmad7 ProteinDose-Response RelationshipYoung AdultPharmacotherapyDouble-Blind MethodDrug TherapyInternal medicineHumansAntisenseGlucocorticoidsAgedDose-Response Relationship Drugbusiness.industryC-reactive proteinNECROSIS-FACTOR-ALPHAOligonucleotides AntisenseTGF-BETA-1-MEDIATED SUPPRESSIONEFFICACYmedicine.diseaseClinical trialMICEbiology.proteinbusinessAdolescent; Adult; Aged; C-Reactive Protein; Crohn Disease; Dose-Response Relationship Drug; Double-Blind Method; Drug Therapy Combination; Female; Glucocorticoids; Humans; Immunosuppressive Agents; Male; Middle Aged; Oligonucleotides; Oligonucleotides Antisense; Remission Induction; Smad7 Protein; Young Adult; Medicine (all)INFLAMMATORY-BOWEL-DISEASE
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