Search results for " Interleukin-10"

showing 10 items of 12 documents

Thyroid Cancer Resistance to Chemotherapeutic Drugs via Autocrine Production of Interleukin-4 and Interleukin-10

2003

We investigated the mechanisms responsible for the widespread refractoriness to chemotherapeutic drugs observed in thyroid cancers. We show that malignant epithelial cells from papillary, follicular, and anaplastic thyroid carcinomas express high levels of Bcl-2 and Bcl-xL. Exogenous expression of either Bcl-2 or Bcl-xL in normal thyrocytes was sufficient to prevent chemotherapeutic drug-induced cytotoxicity. All of the histological thyroid cancer variants examined produced interleukin-4 (IL-4) and interleukin-10 (IL-10), which increased Bcl-2 and Bcl-xL levels and protected thyroid cells from chemotherapeutic agents. Exposure to neutralizing antibodies against IL-4 and IL-10 resulted in do…

Cancer ResearchCell DeathPaclitaxelCancer Research; OncologyCarcinomaThyroid Glandbcl-X ProteinAntineoplastic AgentsApoptosisThyroid Cancer Interleukin-4 Interleukin-10Middle AgedCarcinoma PapillaryInterleukin-10OncologyProto-Oncogene Proteins c-bcl-2Settore MED/04 - PATOLOGIA GENERALEDoxorubicinDrug Resistance NeoplasmHumansInterleukin-4Thyroid NeoplasmsCisplatinAged
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Disrupting immune regulation incurs transient costs in male reproductive function.

2014

9 pages; International audience; BACKGROUND: Immune protection against pathogenic organisms has been shown to incur costs. Previous studies investigating the cost of immunity have mostly focused on the metabolic requirements of immune maintenance and activation. In addition to these metabolic costs, the immune system can induce damage to the host if the immune response is mis-targeted or over-expressed. Given its non-specific nature, an over-expressed inflammatory response is often associated with substantial damage for the host. Here, we investigated the cost of an over-expressed inflammatory response in the reproductive function of male mice. METHODOLOGY/PRINCIPAL FINDINGS: We experimenta…

Genetics and Molecular Biology (all)0106 biological sciencesMalemedicine.medical_treatmentlcsh:MedicineBiochemistry01 natural sciencesMiceMonoclonalReceptorsTestis[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/Symbiosis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyReceptors Interleukin-10Animals; Antibodies Monoclonal; Body Weight; Inflammation; Male; Mice; Organ Size; Receptors Interleukin-10; Reproduction; Spermatozoa; Testis; Immunomodulation; Medicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)lcsh:ScienceReceptorImmune Response0303 health sciencesMultidisciplinaryReproductive functionMedicine (all)ReproductionAging and ImmunityAntibodies MonoclonalOrgan SizeSpermatozoaInterleukin-103. Good healthCytokineCytokines[SDV.IMM]Life Sciences [q-bio]/Immunologymedicine.symptomResearch ArticleInfertilityEvolutionary ImmunologyImmunologyInflammationBiology010603 evolutionary biologyImmune SuppressionAntibodiesImmunomodulation03 medical and health sciencesImmune systemImmunitymedicineAnimalsBiology030304 developmental biologyInflammationEvolutionary Biology[ SDE.BE ] Environmental Sciences/Biodiversity and Ecologylcsh:RBody WeightImmunityImmunoregulationmedicine.diseaseBlockadeAgricultural and Biological Sciences (all)Immune SystemImmunologyHumoral Immunitylcsh:Q[SDE.BE]Environmental Sciences/Biodiversity and Ecology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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Association of interleukin-10G microsatellite polymorphism with the susceptibility of ankylosing spondylitis

2013

Study suggests an association of IL10.G poly- morphisms with AS which might contribute to the increased or decreased susceptibility to AS. IL10.G8 and G7 microsatellites alleles appear as protective alleles against the development of AS in the German subjects investigated here. Allele IL10.G9 seems to be a risk factor for the development of AS. This protective effect of variant promoter alleles could be related to differences in IL- 10 production, which may be clinically relevant.

musculoskeletal diseasesAdultMalechemical and pharmacologic phenomenaRheumatologyimmune system diseasesparasitic diseasesmedicineHumansGenetic Predisposition to DiseaseSpondylitis AnkylosingAnkylosing spondylitisPolymorphism Geneticbusiness.industryIL10 microsatellite polymorphisms ankylosing spondylitisInterleukinhemic and immune systemsJoint boneMiddle Agedmedicine.diseaseInterleukin-10Interleukin 10ImmunologyMicrosatelliteFemalebusinessAnkylosing spondylitis; Interleukin-10; Microsatellite polymorphismsMicrosatellite RepeatsJoint Bone Spine
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Suppressing an Anti-Inflammatory Cytokine Reveals a Strong Age-Dependent Survival Cost in Mice

2010

7 pages; International audience; BACKGROUND: The central paradigm of ecological immunology postulates that selection acts on immunity as to minimize its cost/benefit ratio. Costs of immunity may arise because the energetic requirements of the immune response divert resources that are no longer available for other vital functions. In addition to these resource-based costs, mis-directed or over-reacting immune responses can be particularly harmful for the host. In spite of the potential importance of immunopathology, most studies dealing with the evolution of the immune response have neglected such non resource-based costs. To keep the immune response under control, hosts have evolved regulat…

Male0106 biological sciencesSurvivalmedicine.medical_treatmentAnti-Inflammatory AgentsImmunology/ImmunomodulationDown-Regulationlcsh:MedicineInflammationBiology[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology010603 evolutionary biology01 natural sciencesAntibodiesMice03 medical and health sciencesImmune systemImmunityImmunopathologymedicineAnimalsReceptors Interleukin-10lcsh:ScienceReceptor030304 developmental biologyInflammationEvolutionary Biology[ SDE.BE ] Environmental Sciences/Biodiversity and Ecology0303 health sciencesMultidisciplinarylcsh:RAge FactorsInterleukin-103. Good healthMice Inbred C57BLInterleukin 10CytokineEcology/Physiological Ecology[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyImmunologybiology.proteinlcsh:Q[SDE.BE]Environmental Sciences/Biodiversity and Ecologymedicine.symptomAntibodyResearch ArticlePLoS ONE
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IL-10 and IL-10 receptor overexpression in oral giant cell lesions

2010

Objective: Central giant cell lesions (CGCL) and peripheral giant cell lesions (PGCL) occur in the jaws and contain osteoclast-like giant cells and mononuclear cells positive for the macrophage marker CD68. The participation of immune-inflammatory mechanisms has been proposed in the lesions development. As IL-10 is one of the most important anti-inflammatory cytokines and it is also an inhibitory cytokine to macrophage function and bone resorption, the purpose of the present study was to investigate its expression together with its receptor (IL-10R?) in CGCL and PGCL. Study Design: Six fragments of CGCL and seven fragments of PGCL were obtained by surgical excision. Frozen specimens were cu…

AdultMalePathologymedicine.medical_specialtymedicine.medical_treatmentBiologyPeripheral blood mononuclear cellProinflammatory cytokineYoung AdultGranuloma Giant CellmedicineHumansMacrophageReceptors Interleukin-10ChildGeneral DentistryCD68Middle Agedmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Interleukin-10Interleukin 10CytokineOtorhinolaryngologyGiant cellGranulomaUNESCO::CIENCIAS MÉDICASFemaleSurgeryMouth Diseases
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Budesonide increases TLR4 and TLR2 expression in Treg lymphocytes of allergic asthmatics

2015

Abstract Background Reduced innate immunity responses as well as reduced T regulatory activities characterise bronchial asthma. Objectives In this study the effect of budesonide on the expression of TLR4 and TLR2 in T regulatory lymphocyte sub-population was assessed. Methods TLR4 and TLR2 expression in total peripheral blood mononuclear cells (PBMC), in CD4+/CD25+ and in CD4+/CD25− was evaluated, by flow cytometric analysis, in mild intermittent asthmatics (n = 14) and in controls (n = 11). The in vitro effects of budesonide in modulating: TLR4 and TLR2 expression in controls and in asthmatics; IL-10 expression and cytokine release (IL-6 and TNF-α selected by a multiplex assay) in asthmati…

AdultMalePulmonary and Respiratory MedicineBudesonidemedicine.medical_treatmentLymphocyteIn Vitro TechniquesCorticosteroids; Immunoregulation; T lymphocytes; TLR; Adult; Asthma; Budesonide; Cytokines; Female; Flow Cytometry; Glucocorticoids; Humans; In Vitro Techniques; Interleukin-10; Leukocytes Mononuclear; Male; T-Lymphocytes Regulatory; Toll-Like Receptor 2; Toll-Like Receptor 4; Young Adult; Pulmonary and Respiratory Medicine; Pharmacology (medical); Biochemistry (medical); Medicine (all)T-Lymphocytes RegulatoryPeripheral blood mononuclear cellYoung AdultGlucocorticoidTLRT lymphocytemedicineCorticosteroidHumansPharmacology (medical)IL-2 receptorBudesonideCytokineGlucocorticoidsIn Vitro Techniquebusiness.industryMedicine (all)Biochemistry (medical)ImmunoregulationFlow CytometryAsthmaToll-Like Receptor 2Interleukin-10Toll-Like Receptor 4Interleukin 10TLR2Cytokinemedicine.anatomical_structureImmunologyLeukocytes MononuclearTLR4CytokinesFemalebusinessHumanmedicine.drugPulmonary Pharmacology & Therapeutics
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Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
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MYD88 L265P mutation and interleukin‐10 detection in cerebrospinal fluid are highly specific discriminating markers in patients with primary central …

2021

Reliable biomarkers are needed to avoid diagnostic delay and its devastating effects in patients with primary central nervous system (CNS) lymphoma (PCNSL). We analysed the discriminating sensitivity and specificity of myeloid differentiation primary response (88) (MYD88) L265P mutation (mut-MYD88) and interleukin-10 (IL-10) in cerebrospinal fluid (CSF) of both patients with newly diagnosed (n = 36) and relapsed (n = 27) PCNSL and 162 controls (118 CNS disorders and 44 extra-CNS lymphomas). The concordance of MYD88 mutational status between tumour tissue and CSF sample and the source of ILs in PCNSL tissues were also investigated. Mut-MYD88 was assessed by TaqMan-based polymerase chain reac…

AdultMalePathologymedicine.medical_specialtyLymphomaBiopsyConcordanceinterleukin-10diffuse large B-cell lymphomaMutation MissenseCentral Nervous System Neoplasms03 medical and health sciencesprimary CNS lymphoma0302 clinical medicineCerebrospinal fluidhemic and lymphatic diseasesBiopsyBiomarkers TumorTaqManmedicineHumansdiffuse large B-cell lymphoma interleukin-10 interleukin-6 MYD88 L265P mutation primary CNS lymphomaProspective cohort studyAgedmedicine.diagnostic_testbusiness.industryinterleukin-6Primary central nervous system lymphomaHematologyMiddle Agedmedicine.diseaseInterleukin-10Neoplasm ProteinsLymphomaMYD88 L265P mutationAmino Acid Substitution030220 oncology & carcinogenesisMyeloid Differentiation Factor 88FemalebusinessDiffuse large B-cell lymphoma030215 immunologyBritish Journal of Haematology
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MUC1 oncoprotein promotes refractoriness to chemotherapy in thyroid cancer cells.

2007

Abstract Overexpression of MUC1 oncoprotein is frequently observed in cancer and contributes to confer resistance to genotoxic agents. Papillary, follicular, and anaplastic thyroid carcinomas are the three forms of thyroid epithelial cancer. Anaplastic tumors are less differentiated and extremely aggressive, characterized by a poor prognosis. Little is known about the role of MUC1 in thyroid cancer. We recently showed that autocrine production of interleukin (IL)-4 and IL-10 controls thyroid cancer cell survival, growth, and resistance to chemotherapy through activation of Janus-activated kinase/signal transducers and activators of transcription (JAK/STAT) and phosphatidylinositide 3′-OH ki…

Cancer ResearchTranscription GeneticDrug ResistanceApoptosisSuppressor of Cytokine Signaling ProteinsnPhosphatidylinositol 3-KinasesAntibioticsMedicineRNA Small InterferingThyroid cancerTumorAntibiotics AntineoplasticThyroidAntineoplasticInterleukin-10Mitochondriamedicine.anatomical_structureOncologyTranscriptionSignal TransductionDown-RegulationSmall InterferingTransfectionCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinGeneticSettore MED/04 - PATOLOGIA GENERALEAntigens NeoplasmCell Line TumorHumansThyroid NeoplasmsAnaplastic thyroid cancerAntigensProtein kinase BPI3K/AKT/mTOR pathwayAntibiotics Antineoplastic; Antigens Neoplasm; Apoptosis; Cell Line Tumor; Down-Regulation; Doxorubicin; Drug Resistance Neoplasm; Humans; Interleukin-10; Interleukin-4; Mitochondria; Mucin-1; Mucins; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA Small Interfering; Signal Transduction; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Transcription Genetic; Transfection; Cancer Research; Oncologybusiness.industryMucin-1MucinsCancermedicine.diseaseDoxorubicinDrug Resistance NeoplasmCancer cellCancer researchNeoplasmRNAInterleukin-4businessProto-Oncogene Proteins c-aktCancer research
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Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

2017

Mast cells (MCs) are innate immune cells that exert positive and negative immune modulatory functions capable to enhance or limit the intensity and/or duration of adaptive immune responses. Although MCs are crucial to regulate T cell immunity, their action in the pathogenesis of autoimmune diseases is still debated. Here we demonstrate that MCs play a crucial role in T1D pathogenesis so that their selective depletion in conditional MC knockout NOD mice protects them from the disease. MCs of diabetic NOD mice are overly inflammatory and secrete large amounts of IL-6 that favors differentiation of IL-17-secreting T cells at the site of autoimmunity. Moreover, while MCs of control mice acquire…

0301 basic medicineBlood GlucoseAutoimmune diabeteAutoimmunityNodmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityImmune toleranceSettore MED/13 - EndocrinologiaMiceAutoimmune diabetes0302 clinical medicineMice Inbred NODImmunology and AllergyNOD miceMice KnockoutInterleukin-17Forkhead Transcription FactorsFlow CytometryImmunohistochemistryhumanitiesInterleukin-10Interleukin 10Tumor necrosis factor alphaImmunologySettore MED/50 - Scienze Tecniche Mediche ApplicateMice TransgenicLaser Capture MicrodissectionReal-Time Polymerase Chain Reactionbehavioral disciplines and activities03 medical and health sciencesIslets of LangerhansImmune systemChymasesmedicineAnimalsInflammationInnate immune systembusiness.industryInterleukin-6Immune toleranceSettore MED/46 - Scienze Tecniche di Medicina di LaboratorioAutoimmune diabetes; Immune tolerance; Interleukin-10; Interleukin-6; Mast cells030104 developmental biologyDiabetes Mellitus Type 1ImmunologyMast cellsTh17 CellsMast cells; Autoimmune diabetes; Interleukin-6; Immune tolerance; Interleukin-10business030215 immunology
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