Search results for "interleukin"

showing 10 items of 1856 documents

P38 MAP Kinase Signaling Is Required for the Conversion of CD4+CD25− T Cells into iTreg

2008

CD4+CD25+ regulatory T cells (Treg) are important mediators of immune tolerance. A subset of Treg can be generated in the periphery by TGF-beta dependent conversion of conventional CD4+CD25− T cells into induced Treg (iTreg). In chronic viral infection or malignancy, such induced iTreg, which limit the depletion of aberrant or infected cells, may be of pathogenic relevance. To identify potential targets for therapeutic intervention, we investigated the TGF-beta signaling in Treg. In contrast to conventional CD4+ T cells, Treg exhibited marked activation of the p38 MAP kinase pathway. Inhibition of p38 MAP kinase activity prevented the TGF-beta-dependent conversion of CD4+CD25− T cells into …

MAPK/ERK pathwayp38 mitogen-activated protein kinasesImmunologyBlotting WesternImmunology/Immunomodulationlcsh:MedicineImmunology/Autoimmunitychemical and pharmacologic phenomenaBiologyT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesImmune toleranceImmunology/Leukocyte Signaling and Gene ExpressionMiceAnimalsIL-2 receptorlcsh:ScienceMultidisciplinarylcsh:RInterleukin-2 Receptor alpha SubunitFOXP3hemic and immune systemsFlow CytometryCell biologyMitogen-activated protein kinaseCD4 Antigensbiology.proteinPhosphorylationlcsh:QSignal transductionResearch ArticleSignal TransductionPLoS ONE
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Activation of MAP kinase p38 is critical for the cell-cycle–controlled suppressor function of regulatory T cells

2007

AbstractRegulatory T cells play an essential role in the control of self-tolerance and processes of adaptive immunity. Tolerogenic IL-10–modulated human dendritic cells (IL-10DCs) induce anergic T cells with strong suppressive properties (iTregs) that inhibit the activation of effector T cells. In this study, we evaluated the interaction between cell-cycle regulation and intracellular signaling in these iTregs. Analysis of signal transduction events revealed a down-regulation of the mitogen-activated protein kinases (MAPKs) Jun N-terminal kinase (JNK) and a nonactivation of extracellular-signal–regulated kinase (ERK) in contrast to a marked activation of p38 MAPK and the p38 effector MAPK-a…

MAPK/ERK pathwayp38 mitogen-activated protein kinasesImmunologyIn Vitro TechniquesProtein Serine-Threonine KinasesBiologyT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesBiochemistryAldesleukinHumansProtein kinase AMitogen-Activated Protein Kinase KinasesKinaseCell CycleIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyHematologyAcquired immune systemInterleukin-10Cell biologyMitogen-activated protein kinasebiology.proteinSignal transductionCyclin-Dependent Kinase Inhibitor p27Blood
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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Choice of second-line disease-modifying antirheumatic drugs after failure of methotrexate therapy for rheumatoid arthritis: A decision tree for clini…

2009

Objective To survey rheumatologists' preferences for the choice of a second-line disease-modifying antirheumatic drug (DMARD) after inadequate response with methotrexate (MTX) therapy in rheumatoid arthritis (RA). Methods Thirty-six rheumatologists stated their preferences for RA treatment after inadequate response with MTX therapy (optimal dose at least 6 months). From the initial scenario, we derived 54 vignettes varying by rheumatoid factor or anti–cyclic citrullinated peptide antibody presence, swollen joint count, Disease Activity Score in 28 joints, and structural damage. Respondents stated their preference among 5 therapeutic options: MTX continuation, switch to another conventional …

MESH: Antirheumatic AgentsMESH: Decision TreesMESH: Treatment FailureArthritisMESH: Antibodies Anti-IdiotypicMESH: Logistic ModelsLogistic regressionSeverity of Illness IndexArthritis Rheumatoid0302 clinical medicineimmune system diseasesImmunology and AllergyMESH: Data CollectionPharmacology (medical)Treatment Failure030212 general & internal medicinePractice Patterns Physicians'skin and connective tissue diseasesMESH: Arthritis RheumatoidData CollectionAntibodies Anti-Idiotypic3. Good healthMESH: Interleukin 1 Receptor Antagonist ProteinMESH: Methotrexate[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemAntirheumatic AgentsRheumatoid arthritismedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyMESH: Rheumatoid FactorImmunologyPeptides Cyclic03 medical and health sciencesRheumatologyRheumatoid FactorMESH: Severity of Illness IndexInternal medicineSeverity of illnessmedicineHumansRheumatoid factorMESH: Physician's Practice PatternsMESH: Peptides Cyclic030203 arthritis & rheumatologyAnakinraMESH: HumansTumor Necrosis Factor-alphabusiness.industryDecision Treesmedicine.diseaseRheumatologyInterleukin 1 Receptor Antagonist ProteinLogistic ModelsMethotrexateMESH: Tumor Necrosis Factor-alphaPhysical therapyMethotrexatebusinessArthritis & Rheumatism
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

2012

Among several peroxisomal neurodegenerative disorders, the pseudoneonatal adrenoleukodystrophy (P-NALD) is characterized by the acyl-coenzyme A oxidase 1 (ACOX1) deficiency, which leads to the accumulation of very-long-chain fatty acids ( VLCFA) and inflammatory demyelination. However, the components of this inflammatory process in P-NALD remain elusive. In this study, we used transcriptomic profiling and PCR array analyses to explore inflammatory gene expression in patient fibroblasts. Our results show the activation of IL-1 inflammatory pathway accompanied by the increased secretion of two IL-1 target genes, IL-6 and IL-8 cytokines. Human fibroblasts exposed to very-long-chain fatty acids…

MESH: Inflammationperoxisomal disordersMESH: Osteopontinmedicine.medical_treatmentMESH : ImmunohistochemistryMESH : Transcriptomechemokine receptorsVoeding Metabolisme en Genomica0302 clinical medicineEndocrinologyMESH: Reverse Transcriptase Polymerase Chain ReactionAcyl-CoA oxidasemultiple-sclerosis lesionsMESH : OsteopontinMESH : Fatty AcidsCells CulturedOligonucleotide Array Sequence Analysis[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism0303 health sciencesOxidase testMESH : Gene Expression RegulationReverse Transcriptase Polymerase Chain ReactionFatty AcidsMESH: Acyl-CoA OxidaseMESH : Reverse Transcriptase Polymerase Chain ReactionPeroxisome[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryMESH: Gene Expression RegulationMetabolism and Genomics3. Good healthMESH: Fatty AcidsMESH : Oligonucleotide Array Sequence AnalysisCytokineMetabolisme en GenomicaACOX1AdrenoleukodystrophyNutrition Metabolism and GenomicsMESH : Acyl-CoA Oxidasemedicine.symptomInflammation MediatorsMESH: Cells Culturedmedicine.medical_specialtyMESH : Interleukin-8MESH : Interleukin-6MESH: Inflammation MediatorsInflammationBiologyin-vitroMESH : Interleukin-1MESH : Inflammation Mediators03 medical and health sciencesVoedingInternal medicinePeroxisomal disordernf-kappa-bMESH : Cells CulturedMESH : Fibroblastsmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologygene[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyNutrition030304 developmental biologyVLAGInflammationMESH: HumansMESH : InflammationInterleukin-6MESH: TranscriptomeInterleukin-8MESH : HumansMESH: Interleukin-1MESH: ImmunohistochemistryFibroblastsmedicine.diseaseMESH: Interleukin-6MESH: Interleukin-8EndocrinologyGene Expression RegulationMESH: FibroblastsMESH: Oligonucleotide Array Sequence AnalysiscellsBrief ReportsOsteopontinmicroarray analysisAcyl-CoA OxidaseTranscriptomeinterleukin-1030217 neurology & neurosurgeryx-linked adrenoleukodystrophyInterleukin-1
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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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Human OX40 tunes the function of regulatory T cells in tumor and nontumor areas of hepatitis C virus-infected liver tissue.

2014

International audience; Regulatory T cells (Tregs) can be considered as a mixed population of distinct subsets, endowed with a diverse extent and quality of adaptation to microenvironmental signals. Here, we uncovered an opposite distribution of Treg expansion, phenotype, and plasticity in different microenvironments in the same organ (liver) derived from patients with chronic hepatitis C: On the one side, cirrhotic and tumor fragments were moderately and highly infiltrated by Tregs, respectively, expressing OX40 and a T-bet high IFN-c – " T-helper (Th)1-suppressing " phenotype; on the other side, noncirrhotic liver specimens contained low frequencies of Tregs that expressed low levels of O…

MESH: Receptors OX40/metabolism*MESH: Interleukin-12/metabolismLiver CirrhosisMaleMacrophagemedicine.disease_causeMESH: Carcinoma Hepatocellular/immunology*T-Lymphocytes RegulatoryMESH: OX40 Ligand/metabolism0302 clinical medicineMESH: Aged 80 and overMESH: T-Lymphocytes Regulatory/physiology*MESH: Up-RegulationOX40MESH: AgedAged 80 and over0303 health scienceseducation.field_of_studyT REGMESH: Middle AgedMedicine (all)MESH: Liver Cirrhosis/immunology*Liver Neoplasmshemic and immune systemsMiddle AgedMESH: Liver Neoplasms/immunology*PhenotypeHepatitis CInterleukin-123. Good healthUp-RegulationPhenotypeLiver Neoplasm[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyInterleukin 12[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemalemedicine.symptomMESH: Hepatitis C/immunology*OX40; T REG; HEPATITIS C VIRUSHumanmedicine.medical_specialtyCarcinoma HepatocellularHepatitis C virusLiver CirrhosiPopulationInflammationchemical and pharmacologic phenomena[SDV.CAN]Life Sciences [q-bio]/CancerOX40 LigandBiologyMESH: PhenotypeMESH: Liver Neoplasms/virology03 medical and health sciencesIkaros Transcription FactorDownregulation and upregulationInternal medicinemedicineHumansMESH: Macrophages/metabolismeducation030304 developmental biologyAgedMESH: HumansHepatologyMacrophagesHEPATITIS C VIRUSMESH: Carcinoma Hepatocellular/virologyHepatologyReceptors OX40MESH: Ikaros Transcription Factor/metabolismMESH: Hepatitis C/complicationsMESH: MaleOX40 ligandImmunologyMESH: Liver Cirrhosis/virologyMESH: Female030215 immunology
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A newly established murine immature dendritic cell line can be differentiated into a mature state, but exerts tolerogenic function upon maturation in…

2007

AbstractThe phenotype and function of murine dendritic cells (DCs) are primarily studied using bone-marrow–derived DCs (BM-DCs), but may be hampered by the heterogenous phenotype of BM-DCs due to their differential state of maturation. Here we characterize a newly established murine DC line (SP37A3) of myeloid origin. During maintainance in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and M-CSF, SP37A3 cells resemble immature DCs characterized by low expression of major histocompatibility complex (MHC) II and costimulatory molecules and low T-cell stimulatory capacity. Upon stimulation, SP37A3 cells acquire a mature phenotype and activate naive T cells as potent…

Macrophage colony-stimulating factorMyeloidmedicine.medical_treatmentImmunologyBiologyMajor histocompatibility complexT-Lymphocytes RegulatoryBiochemistryDexamethasoneCell LineMicemedicineAnimalsGlucocorticoidsMyeloid Progenitor CellsCell ProliferationClonal AnergyMice Inbred BALB CFollicular dendritic cellsReceptors IgGHistocompatibility Antigens Class IICell DifferentiationDendritic CellsCell BiologyHematologyDendritic cellCoculture TechniquesUp-RegulationCell biologyInterleukin 1 Receptor Antagonist ProteinGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureCytokineCell culturebiology.proteinCytokinesmedicine.drugBlood
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Production of macrophage-, granulocyte-, granulocyte-macrophage- and multi-colony-stimulating factor by peripheral blood cells

1989

The specific cell sources and signals for induction of various colony-stimulating factors (CSF) in peripheral blood mononuclear cells (PBMC), purified T lymphocyte and monocyte (Mo) populations have been investigated. In the absence of exogenous activating stimuli, human PBMC, T cells and Mo failed to produce stable cytoplasmic mRNA for CSF for macrophages (M-CSF or CSF-1), for granulocytes (G-CSF), for granulocytes and macrophages (GM-CSF) and for multilineage CSF [multi-CSF, interleukin (IL) 3] and thus failed to release CSF proteins. However, after stimulation with phorbol myristate acetate and phytohemagglutinin, M-, G-, GM- and multi-CSF mRNA became detectable in PBMC, resulting in the…

Macrophage colony-stimulating factorT-Lymphocytesmedicine.medical_treatmentImmunologyGranulocyteBiologyPeripheral blood mononuclear cellMonocytesColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineHumansImmunology and AllergyMacrophageRNA MessengerGrowth SubstancesMacrophage Colony-Stimulating FactorMonocyteGranulocyte-Macrophage Colony-Stimulating FactorT lymphocyteMolecular biologyGranulocyte macrophage colony-stimulating factorCytokinemedicine.anatomical_structureImmunologyInterleukin-3medicine.drugEuropean Journal of Immunology
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