Search results for "RAR-related orphan receptor gamma"

showing 10 items of 15 documents

Chemopreventive effect of oleuropein in colitis-associated colorectal cancer in c57bl/6 mice

2015

Scope The main phenolic secoiridoid oleuropein and active constituent from olive tree (Olea europaea, Oleaceae), has demonstrated anti-inflammatory properties in intestinal inflammation and anti-tumoral effects in different cancer cells. In this study, we evaluated the chemoprevention of oleuropein in a model of azoxymethane (AOM)/Dextran sulfate sodium (DSS)-induced colorectal cancer (CRC) in C57BL/6 mice and the modulatory effect on the Th17 response in DSS acute colitis. Methods and results Oleuropein protected from AOM/DSS-induced CRC by improving clinical symptoms, disease activity index score as well as suppressed the growth and multiplicity of colonic tumors. Treatment with oleuropei…

0301 basic medicineColonColorectal cancerIridoid GlucosidesAzoxymethanePharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOleuropeinRAR-related orphan receptor gammamedicineAnimalsAnticarcinogenic AgentsIridoidsColitisProtein kinase BAcute colitisCell ProliferationChemistryAzoxymethaneDextran SulfateNeoplasms ExperimentalColitismedicine.diseaseMice Inbred C57BL030104 developmental biology030220 oncology & carcinogenesisImmunologyCancer cellCytokinesTh17 CellsFemaleColorectal NeoplasmsFood ScienceBiotechnologyMolecular Nutrition & Food Research
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Targeting cellular fatty acid synthesis limits T helper and innate lymphoid cell function during intestinal inflammation and infection

2019

CD4+ T cells contribute critically to a protective immune response during intestinal infections, but have also been implicated in the aggravation of intestinal inflammatory pathology. Previous studies suggested that T helper type (Th)1 and Th17 cells depend on de novo fatty acid (FA) synthesis for their development and effector function. Here, we report that T-cell-specific targeting of the enzyme acetyl-CoA carboxylase 1 (ACC1), a major checkpoint controlling FA synthesis, impaired intestinal Th1 and Th17 responses by limiting CD4+ T-cell expansion and infiltration into the lamina propria in murine models of colitis and infection-associated intestinal inflammation. Importantly, pharmacolog…

0301 basic medicineImmunologyBiologyMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemRAR-related orphan receptor gammamedicineAnimalsImmunology and AllergyFatty acid synthesisBarrier functionLamina propriaEffectorFatty AcidsInnate lymphoid cellT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3ColitisInflammatory Bowel DiseasesImmunity InnateBiosynthetic PathwaysDisease Models Animal030104 developmental biologymedicine.anatomical_structurechemistryImmunologyLipogenesisBiomarkersAcetyl-CoA Carboxylase030215 immunologyMucosal Immunology
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IL-17 polarization of MAIT cells is derived from the activation of two different pathways

2017

MAIT cells are expanded in salivary glands of patients with Sjogren's syndrome and are IL-17 polarized. IL-7 and IL-23 induce IL-17 production activating two different pathways: IL-7 stimulation induces in fact a significant STAT3 and HIF1alpha upregulation, conversely, IL-23 stimulation significantly induces RORc overexpression in MAIT cells of patients with Sjogren's syndrome.

0301 basic medicineImmunologyStimulationInterleukin-23Mucosal-Associated Invariant T CellsSalivary GlandsSTAT303 medical and health sciencesIL-17; IL-23; IL-7; MAIT cells; RORc; Sjogren's Syndrome; STAT3; Immunology and Allergy; Immunology0302 clinical medicinestomatognathic systemDownregulation and upregulationRAR-related orphan receptor gammaIL-23Interleukin 23HumansImmunology and AllergySTAT3MAIT cellIL-7biologyInterleukin-17MAIT CellsCell biologyRORcIL-17Settore MED/16 - Reumatologia030104 developmental biologySjogren's Syndromebiology.proteinInterleukin 17030215 immunology
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A Weaning Reaction to Microbiota Is Required for Resistance to Immunopathologies in the Adult.

2019

International audience; Microbes colonize all body surfaces at birth and participate in the development of the immune system. In newborn mammals, the intestinal microbiota is first shaped by the dietary and immunological components of milk and then changes upon the introduction of solid food during weaning. Here, we explored the reactivity of the mouse intestinal immune system during the first weeks after birth and into adulthood. At weaning, the intestinal microbiota induced a vigorous immune response—a “weaning reaction”—that was programmed in time. Inhibition of the weaning reaction led to pathological imprinting and increased susceptibility to colitis, allergic inflammation, and cancer …

0301 basic medicinecolitis[SDV]Life Sciences [q-bio]short-chain fatty acidsImmunologyRetinoic acidTretinoinWeaningBiologyT-Lymphocytes Regulatoryregulatory T cellsAllergic inflammation03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineImmune systemRAR-related orphan receptor gammamicrobiotamedicineImmunology and AllergyWeaningAnimalsinflammatory pathologyColitisImprinting (psychology)Intestinal Mucosaneonatal periodNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseFatty Acids Volatile3. Good healthGastrointestinal Microbiome[SDV] Life Sciences [q-bio]Mice Inbred C57BL030104 developmental biologyInfectious DiseaseschemistryAnimals NewbornSolid food030220 oncology & carcinogenesisImmunologymucosal immunityImmunity
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Tissue microenvironment dictates the fate and tumor-suppressive function of type 3 ILCs

2017

Nussbaum et al. found that tumor suppression through innate lymphoid cells (ILCs) cannot be predicted solely based on the ILC phenotype and lineage but that their immune properties are shaped both by their ontogeny and by the tissue microenvironment they reside in.

0301 basic medicinemedicine.medical_treatmentImmunology314610 Medicine & healthBiology10263 Institute of Experimental ImmunologyArticle31103 medical and health sciencesMiceRAR-related orphan receptor gammaCell Line TumormedicineImmunology and AllergyAnimalsLymphocytesskin and connective tissue diseasesTranscription factorResearch ArticlesMice Knockout2403 ImmunologyInnate lymphoid cellNeoplasms ExperimentalNuclear Receptor Subfamily 1 Group F Member 3PhenotypeCell biologybody regionsKiller Cells NaturalMice Inbred C57BL030104 developmental biologyCytokineCellular MicroenvironmentCell cultureTumor progressionInterleukin 122723 Immunology and AllergyCytokines570 Life sciences; biologyTranscription Factors
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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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Type 1 diabetic mellitus patients with increased atherosclerosis risk display decreased CDKN2A/2B/2BAS gene expression in leukocytes

2019

Background Type 1 diabetes mellitus (T1DM) patients display increased risk of cardiovascular disease (CVD) and are characterized by a diminished regulatory T (Treg) cell content or function. Previous studies have shown an association between decreased CDKN2A/2B/2BAS gene expression and enhanced CVD. In the present study the potential relationship between CDKN2A/2B/2BAS gene expression, immune cell dysfunction and increased cardiovascular risk in T1DM patients was explored. Methods A cross-sectional study was performed in 90 subjects divided into controls and T1DM patients. Circulating leukocyte subpopulations analysis by flow cytometry, expression studies on peripheral blood mononuclear cel…

Blood Glucose0301 basic medicineendocrine system diseasesCellular differentiationlcsh:Medicine0302 clinical medicineRisk FactorsRAR-related orphan receptor gammaimmune system diseasesLeukocytesIL-2 receptorDiabetisFOXP3Cell DifferentiationGeneral MedicineType 1 diabetes030220 oncology & carcinogenesisCytokinesRNA Long Noncodingmedicine.symptomAdultmedicine.medical_specialtyCD14T cellsInflammationPeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInternal medicinemedicineHumansRNA MessengerCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15Glycated HemoglobinInflammationType 1 diabetesbusiness.industryResearchlcsh:RAtherosclerosismedicine.diseaseCardiovascular riskDiabetes Mellitus Type 1030104 developmental biologyEndocrinologyGene Expression RegulationCase-Control StudiesbusinessJournal of Translational Medicine
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The protein tyrosine kinase Tec regulates a CD44highCD62L- Th17 subset.

2010

Abstract The generation of Th17 cells has to be tightly controlled during an immune response. In this study, we report an increase in a CD44highCD62L− Th17 subset in mice deficient for the protein tyrosine kinase Tec. CD44highCD62L− Tec−/− CD4+ T cells produced enhanced IL-17 upon activation, showed increased expression levels of IL-23R and RORγt, and IL-23–mediated expansion of Tec−/− CD4+ T cells led to an increased production of IL-17. Tec−/− mice immunized with heat-killed Streptococcus pneumoniae displayed increased IL-17 expression levels in the lung postinfection with S. pneumoniae, and this correlated with enhanced pneumococcal clearance and reduced lung inflammation compared with T…

Encephalomyelitis Autoimmune ExperimentalTECeducationImmunologyImmunoblottingInflammationEnzyme-Linked Immunosorbent AssayCell SeparationBiologyMiceImmune systemIn vivoRAR-related orphan receptor gammaT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsCell LineageL-SelectinMice KnockoutReverse Transcriptase Polymerase Chain ReactionCD44Interleukin-17hemic and immune systemsCell DifferentiationPneumoniaT-Lymphocytes Helper-InducerProtein-Tyrosine KinasesFlow CytometryMolecular biologyHyaluronan ReceptorsCancer researchbiology.proteinCytokinesmedicine.symptomSignal transductiontissuesTyrosine kinaseSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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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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Increased levels of Th17 cells are associated with non-neuronal acetylcholine in COPD patients.

2014

T-lymphocytes, including Th17-cells and T-cells expressing acetylcholine (ACh), are key components of systemic inflammation in chronic obstructive pulmonary disease (COPD). We investigated whether ACh promotes Th17 cells in COPD. ACh, IL-17A, IL-22, RORγt, FOXP3 expression and AChIL-17A, AChIL-22, AChRORγt coexpression was evaluated in peripheral blood mononuclear cells (PBMC) from COPD patients (n=16), healthy smokers (HS) (n=12) and healthy control subjects (HC) (n=13) (cultured for 48 h with PMA) by flow cytometry. Furthermore, we studied the effect of Tiotropium (Spiriva®) (100 nM) and Olodaterol (1nM) alone or in combination, and of hemicholinium-3 (50 μM) on AChIL-17A, AChIL-22, AChRO…

MaleImmunologyIntracellular SpaceScopolamine DerivativesPharmacologySystemic inflammationPeripheral blood mononuclear cellCholinergic AntagonistsFlow cytometrychemistry.chemical_compoundPulmonary Disease Chronic ObstructiveRAR-related orphan receptor gammaRisk FactorsmedicineImmunology and AllergyHumansTiotropium BromideAgedAged 80 and overCOPDmedicine.diagnostic_testbusiness.industryInterleukinsOlodaterolInterleukin-17FOXP3Forkhead Transcription FactorsHematologyMiddle AgedNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseAcetylcholineBenzoxazineschemistryLeukocytes MononuclearTh17 CellsFemalemedicine.symptombusinessAcetylcholinemedicine.drugImmunobiology
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