Search results for "interleukins"

showing 10 items of 137 documents

PLASMATIC SIL 6R/IL-6 RATIO AS APOTENTIAL PREDICTOR OF HIGH GLEASON SUM AT RADICAL PROSTATECTOMY

2012

Background: Approximately 40% of males with low Gleason grade clinically localized prostate cancer (PCa) at biopsy were finally diagnosed with high Gleason grade PCa at radical prostatectomy (RP). Therefore, a more reliable assessment of the Gleason grade prior to RP is required. Readily available modalities such as circulating biomarkers may be useful for this purpose. The aim of this study was to evaluate the ability of preoperative interleukin 6 (IL-6) and its soluble receptor (sIL-6R), as well as urokinase-type plasminogen activator (u- PA), its receptor (u-PAR) and the inhibitor (PAI-1) to predict Gleason score upgrading. Patients and Methods: A total of 51 PCa patients with biopsy Gle…

Prostate cancer interleukins GleasonSettore MED/24 - Urologia
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Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms

2021

Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT iso…

QH301-705.5medicine.medical_treatmentReviewCatalysisstatInorganic ChemistryPulmonary fibrosismedicineHumansProtein IsoformsPhysical and Theoretical ChemistryBiology (General)STAT3Molecular BiologyProtein Kinase InhibitorsQD1-999SpectroscopyCellular SenescenceJanus KinasesbiologyChemistryGrowth factorInterleukinsinterstitial lung disease (ILD)Organic ChemistryJAK-STAT signaling pathwayGeneral Medicinerespiratory systemmedicine.diseaseEndoplasmic Reticulum StressComputer Science Applicationsrespiratory tract diseasesSTAT Transcription FactorsChemistrysignal transducer and activator of transcription (STAT)biology.proteinCancer researchidiopathic pulmonary fibrosis (IPF)Janus kinaseLung Diseases InterstitialJanus kinases (JAK)Platelet-derived growth factor receptorTransforming growth factorSignal TransductionInternational Journal of Molecular Sciences
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Protection from lethal septic peritonitis by neutralizing the biological function of interleukin 27

2006

The immune response to bacterial infections must be tightly controlled to guarantee pathogen elimination while preventing tissue damage by uncontrolled inflammation. Here, we demonstrate a key role of interleukin (IL)-27 in regulating this critical balance. IL-27 was rapidly induced during murine experimental peritonitis induced by cecal ligation and puncture (CLP). Furthermore, mice deficient for the EBI3 subunit of IL-27 were resistant to CLP-induced septic peritonitis as compared with wild-type controls, and this effect could be suppressed by injection of recombinant single-chain IL-27. EBI3−/− mice displayed significantly enhanced neutrophil migration and oxidative burst capacity during…

Recombinant Fusion ProteinsImmunologyDown-RegulationPeritonitisInflammationPeritonitisBiologySepsisMiceImmune systemSepsismedicineAnimalsImmunology and AllergyInterleukin 27Innate immune systemBacteriaInterleukinsBrief Definitive ReportInterleukinReceptors Interleukinmedicine.diseaseImmunity InnateUp-RegulationRespiratory burstMice Inbred C57BLProtein SubunitsSolubilityImmunologyBrief Definitive Reportsmedicine.symptomGranulocytesJournal of Experimental Medicine
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Different profile and distribution of antigen specific T cells induced by intranasal and intrarectal immunization with rotavirus 2/6-VLP with and wit…

2013

International audience; In this study, we compared both the profile and distribution of antigen specific primed T cells after intrarectal (IR) and intranasal (IN) immunization with rotavirus (RV) 2/6-VLP, alone or in the presence of LT-R192G, in order to highlight the differences between the two routes and the impact of the adjuvant. Adult BALB/c mice were immunized once with 2/6-VLP with or without adjuvant and the T cell response was analyzed in lymphoid tissues after in vitro restimulation with the antigen. IN, but not IR, immunization of mice with 2/6-VLP alone induced antigen-specific IL-10 and IL-17 secreting T cells. IL-10-, in contrast to IL-17-, secreting T cells did not migrate to…

Rotavirusmedicine.medical_treatmentT-Lymphocytes[SDV]Life Sciences [q-bio]Priming (immunology)DistributionPHENOTYPEPROTECTSEnterotoxins0302 clinical medicineCell MovementINFECTIONMesenteric lymph nodesHEAT-LABILE TOXINIMMUNE-RESPONSEIL-2 receptorAntigens Viral0303 health sciencesB-LymphocytesMice Inbred BALB CIntrarectalEscherichia coli ProteinsVaccinationFOXP3CHOLERA-TOXINLT-R192G3. Good healthInfectious Diseasesmedicine.anatomical_structureIntranasal030220 oncology & carcinogenesisMolecular MedicineFemaleAdjuvantLymphoid TissueT cellBacterial ToxinsSpleenBiologyMUCOSAL VACCINESRotavirus Infections03 medical and health sciencesCross-PrimingAntigenAdjuvants ImmunologicAdministration RectalVIRUS-LIKE PARTICLESmedicineAnimalsVaccines Virus-Like ParticleImmunity MucosalAdministration Intranasal030304 developmental biologyGeneral VeterinaryGeneral Immunology and MicrobiologyInterleukinsPublic Health Environmental and Occupational HealthRotavirus VaccinesT cellMICEImmunologyCHALLENGE
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Generation of T Follicular Helper Cells Is Mediated by Interleukin-21 but Independent of T Helper 1, 2, or 17 Cell Lineages

2008

After activation, CD4(+) helper T (Th) cells differentiate into distinct effector subsets. Although chemokine (C-X-C motif) receptor 5-expressing T follicular helper (Tfh) cells are important in humoral immunity, their developmental regulation is unclear. Here we show that Tfh cells had a distinct gene expression profile and developed in vivo independently of the Th1 or Th2 cell lineages. Tfh cell generation was regulated by ICOS ligand (ICOSL) expressed on B cells and was dependent on interleukin-21 (IL-21), IL-6, and signal transducer and activator of transcription 3 (STAT3). However, unlike Th17 cells, differentiation of Tfh cells did not require transforming growth factor beta (TGF-beta…

STAT3 Transcription FactorAdoptive cell transferCellular differentiationCellImmunologyGene ExpressionLymphocyte ActivationCXCR5ArticleInducible T-Cell Co-Stimulator LigandMiceInterleukin 21T-Lymphocyte SubsetsTransforming Growth Factor betaFollicular phasemedicineAnimalsCytotoxic T cellImmunology and AllergyCell LineageMOLIMMUNOOligonucleotide Array Sequence AnalysisB-LymphocytesT follicular helper cell differentiationbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingInterleukinsInterleukin-17ProteinsGerminal centerCell DifferentiationT-Lymphocytes Helper-InducerTransforming growth factor betaFlow CytometryGerminal CenterAdoptive TransferImmunohistochemistryMolecular biologyMice Mutant Strainsmedicine.anatomical_structureInfectious DiseasesT helper 1CELLIMMUNOImmunologybiology.proteinInterleukin 17Signal TransductionImmunity
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STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing.

2009

Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific d…

STAT3 Transcription FactorAnimals; Colitis/chemically induced; Colitis/immunology; Dextran Sulfate/pharmacology; Epithelial Cells/cytology; Epithelial Cells/physiology; Gene Expression Profiling; Inflammation/immunology; Inflammation/pathology; Interleukin-6/genetics; Interleukin-6/immunology; Interleukins/genetics; Interleukins/immunology; Intestinal Mucosa/cytology; Intestinal Mucosa/pathology; Mice; Mice Inbred C57BL; Mice Knockout; Oligonucleotide Array Sequence Analysis; STAT3 Transcription Factor/genetics; STAT3 Transcription Factor/metabolism; Signal Transduction/physiology; Wound HealingImmunologyInterleukin 22Mice03 medical and health sciences0302 clinical medicineIntestinal mucosaConditional gene knockoutImmunology and AllergyAnimalsIntestinal MucosaSTAT3Oligonucleotide Array Sequence Analysis030304 developmental biologyInflammationMice KnockoutWound Healing0303 health sciencesbiologyInterleukin-6Gene Expression ProfilingInterleukinsDextran SulfateBrief Definitive ReportEpithelial CellsCell BiologySTAT3 Transcription FactorColitisIntestinal epithelium3. Good healthMice Inbred C57BLbiology.proteinCancer researchSTAT proteinWound healingSignal Transduction030215 immunology
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The interleukin-22/STAT3 pathway potentiates expression of inducible nitric-oxide synthase in human colon carcinoma cells.

2007

Inducible nitric-oxide synthase (iNOS) has been identified as a marker and mediator of disease in human colonic inflammation and carcinogenesis. Accordingly, identification of mediators that trigger iNOS in colon carcinoma/epithelial cells is an important topic of current research. Here we demonstrate that interleukin (IL)-22, a newly described member of the IL-10 cytokine family, potently synergizes with interferon (IFN)-gamma for iNOS expression in human DLD-1 colon carcinoma cells. Detection of both IL-22 receptor chains and STAT3 phosphorylation proved robust IL-22 responsiveness of these cells. Short interfering RNA technology identified STAT3 as being crucial for up-regulation of iNOS…

STAT3 Transcription Factormedicine.medical_treatmentNitric Oxide Synthase Type IIBiologymedicine.disease_causeBiochemistryGene Expression Regulation EnzymologicInterleukin 22InterferonmedicineHumansRNA MessengerRNA NeoplasmSTAT3Promoter Regions GeneticMolecular BiologyInflammationInterleukinsNF-kappa BInterleukinCell BiologyTransfectionReceptors InterleukinMolecular biologyNeoplasm ProteinsGene Expression Regulation NeoplasticCytokineSTAT1 Transcription FactorColonic Neoplasmsbiology.proteinCancer researchCytokinesIntercellular Signaling Peptides and ProteinsTumor necrosis factor alphaImmunotherapyCaco-2 CellsCarcinogenesismedicine.drugSignal TransductionThe Journal of biological chemistry
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Tristetraprolin regulation of interleukin-22 production

2015

AbstractInterleukin (IL)-22 is a STAT3-activating cytokine displaying characteristic AU-rich elements (ARE) in the 3′-untranslated region (3′-UTR) of its mRNA. This architecture suggests gene regulation by modulation of mRNA stability. Since related cytokines undergo post-transcriptional regulation by ARE-binding tristetraprolin (TTP), the role of this destabilizing protein in IL-22 production was investigated. Herein, we demonstrate that TTP-deficient mice display augmented serum IL-22. Likewise, IL-22 mRNA was enhanced in TTP-deficient splenocytes and isolated primary T cells. A pivotal role for TTP is underscored by an extended IL-22 mRNA half-life detectable in TTP-deficient T cells. Lu…

STAT3 Transcription Factormedicine.medical_treatmentT-LymphocytesTristetraprolinPrimary Cell CultureMAP Kinase Kinase 1BiologyJurkat cellsArticleInterleukin 22Jurkat CellsMiceTristetraprolinNitrilesmedicineButadienesAnimalsHumansRNA Messengerddc:610Regulation of gene expressionAU-rich elementAU Rich ElementsInflammationMultidisciplinaryInterleukinsHEK 293 cellsInterleukinCell biologyCytokineHEK293 CellsGene Expression RegulationImmunologyErratumScientific Reports
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Efficacy of a 12-Week Simeprevir Plus Peginterferon/Ribavirin (PR) Regimen in Treatment-Naïve Patients with Hepatitis C Virus (HCV) Genotype 4 (GT4) …

2017

Background HCV GT4 accounts for up to 20% of HCV infections worldwide. Simeprevir, given for 12 weeks as part of a 24- or 48-week combination regimen with PR is approved for the treatment of chronic HCV GT4 infection. Primary study objectives were assessment of efficacy and safety of simeprevir plus PR in treatment-naïve patients with HCV GT4 treated for 12 weeks. Primary efficacy outcome was sustained virologic response 12 weeks post-treatment (SVR12). Additional objectives included investigation of potential associations of rapid virologic response and baseline factors with SVR12. Methods This multicentre, open-label, single-arm study (NCT01846832) evaluated efficacy and safety of simepre…

SimeprevirMalePsychologie appliquéeFetge - MalaltiesHepacivirusGastroenterologyPolyethylene GlycolPolyethylene Glycols0302 clinical medicinelcsh:Science61 - MedicinaLiver DiseasesSciences bio-médicales et agricolesCirrhosisInterferonLiver Fibrosis030211 gastroenterology & hepatologyDrug Therapy CombinationViral loadBiologieHumanmedicine.medical_specialtyCiències multidisciplinàriesGenotypeSaudi ArabiaAlpha interferon:Otros calificadores::Otros calificadores::/farmacoterapia [Otros calificadores]Gastroenterology and HepatologyMicrobiologyAntiviral Agents03 medical and health sciencesHumansAgedMedicine and health sciencesHepaciviruFlavivirusesInterleukinslcsh:ROrganismsInterleukinmedicine.diseaseRegimen:Digestive System Diseases::Liver Diseases [DISEASES]chemistryImmunologylcsh:QMedicaments - AdministracióDevelopmental BiologyRNA viruseslcsh:Medicinemedicine.disease_cause:Other subheadings::Other subheadings::/drug therapy [Other subheadings]Geographical Locationschemistry.chemical_compoundSimeprevirHospital Universitari Vall d’Hebron030212 general & internal medicinePathology and laboratory medicineMultidisciplinaryHepatitis C virusHepatitis CRecombinant ProteinMedical microbiologyMiddle AgedViral LoadHepatitis CRecombinant Proteins:enfermedades del sistema digestivo::enfermedades hepáticas [ENFERMEDADES]EuropeResearch DesignVirusesFemalePathogensResearch ArticleAdultAsiaAdolescentClinical Research DesignHepatitis C virusResearch and Analysis MethodsYoung AdultInternal medicineRibavirinmedicineddc:610Rapid Virologic ResponseAntiviral AgentBiology and life sciencesbusiness.industryRibavirinViral pathogensInterferon-alphaFibrosisHepatitis virusesMicrobial pathogensPeople and PlacesAdverse EventsInterferonsbusinessPLoS ONE
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T helper cell polarisation in coeliac disease: any (T-)bet ?

2004

Recent data strongly support the view that coeliac disease is a Th1 mediated inflammatory disease as both interferon γ production and T-bet levels in gut infiltrating cells are upregulated The puzzling observation on high interferon γ (IFN-γ) but low interleukin (IL)-12 levels in coeliac disease (CD) has resulted in questions about the underlying principles of T helper cell polarisation. In this issue of G ut ,1 the molecular basis of T helper cell polarisation in CD has been illuminated by the finding that T-bet, the master transcription factor of T helper cell type 1 (Th1) cells, is upregulated in this disease [see page 1090] . The past decade has witnessed a dramatic improvement in our p…

T cellInterleukinsGastroenterologyT helper cellCoeliac DiseaseBiologyTh1 CellsGliadinUp-RegulationInterleukin 21Celiac DiseaseInterferon-gammaImmune systemmedicine.anatomical_structureInterleukin 25ImmunologyInterleukin 13medicineCytotoxic T cellCytokinesHumansIL-2 receptorT-Box Domain ProteinsTranscription FactorsGut
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