Search results for "3 T"

showing 10 items of 125 documents

The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

2014

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells d…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCancer ResearchPrimary Cell CultureFollicular lymphomaBiologyParacrine signallingCytosolCell-Derived MicroparticlesInternal medicinemedicineHumansProtein IsoformsPhosphorylationAutocrine signallingLymphoma FollicularCell ProliferationMitogen-Activated Protein Kinase 1B-LymphocytesMitogen-Activated Protein Kinase 3Gene Expression Regulation LeukemicInterleukinsMicrovesicleMedicine (all)Cell MembraneB-LymphocyteGerminal centerOncostatin M receptorInterleukinProtein IsoformReceptors InterleukinHematologyInterleukinMiddle Agedmedicine.diseaseGerminal CenterMolecular biologyCell-Derived MicroparticleEndocrinologySTAT1 Transcription FactorAnesthesiology and Pain MedicineOncologyFemaleSignal transductionNeoplasm GradingProto-Oncogene Proteins c-aktHumanSignal Transduction
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Extracellular Nampt promotes macrophage survival via a nonenzymatic interleukin-6/STAT3 signaling mechanism.

2008

Macrophages play key roles in obesity-associated pathophysiology, including inflammation, atherosclerosis, and cancer, and processes that affect the survival-death balance of macrophages may have an important impact on obesity-related diseases. Adipocytes and other cells secrete a protein called extracellular nicotinamide phosphoribosyltransferase (eNampt; also known as pre-B cell colony enhancing factor or visfatin), and plasma levels of eNampt increase in obesity. Herein we tested the hypothesis that eNampt could promote cell survival in macrophages subjected to endoplasmic reticulum (ER) stress, a process associated with obesity and obesity-associated diseases. We show that eNampt potent…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCell SurvivalNicotinamide phosphoribosyltransferaseApoptosisBiologyEndoplasmic ReticulumBiochemistryStat3 Signaling Pathwaychemistry.chemical_compoundParacrine signallingMicePiperidinesInternal medicinemedicineAnimalsSecretionAutocrine signallingSTAT3Nicotinamide PhosphoribosyltransferaseMolecular BiologyNicotinamide MononucleotideNicotinamide mononucleotideAcrylamidesInterleukin-6MacrophagesMechanisms of Signal TransductionCell BiologyCell biologyMice Inbred C57BLEndocrinologychemistryGene Expression Regulationbiology.proteinCytokinesSignal transductionSignal TransductionThe Journal of biological chemistry
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Interruption of Macrophage-Derived IL-27(p28) Production by IL-10 during Sepsis Requires STAT3 but Not SOCS3

2014

Abstract Severe sepsis and septic shock are leading causes of morbidity and mortality worldwide. Infection-associated inflammation promotes the development and progression of adverse outcomes in sepsis. The effects of heterodimeric IL-27 (p28/EBI3) have been implicated in the natural course of sepsis, whereas the molecular mechanisms underlying the regulation of gene expression and release of IL-27 in sepsis are poorly understood. We studied the events regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal ligation and puncture. Neutralizing Abs to IL-27(p28) improved survival rates, restricted cytokine release, and reduced bacterial burden in C57BL/…

MaleSTAT3 Transcription Factormedicine.medical_treatmentImmunologySuppressor of Cytokine Signaling ProteinsInflammationSpleenBiologyArticleSepsisMiceSepsismedicineAnimalsHumansImmunology and AllergyReceptors CytokineAntibodies BlockingCecumCells CulturedMice KnockoutSeptic shockInterleukinsMacrophagesReceptors Interleukinmedicine.diseaseBacterial LoadInterleukin-10Mice Inbred C57BLToll-Like Receptor 4Adaptor Proteins Vesicular TransportDisease Models AnimalOxidative StressInterleukin 10Cytokinemedicine.anatomical_structureIntegrin alpha MSuppressor of Cytokine Signaling 3 ProteinMyeloid Differentiation Factor 88ImmunologyTLR4biology.proteinmedicine.symptomJournal of Immunology
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Interleukin (IL)-22 receptor 1 is over-expressed in primary Sjogren's syndrome and Sjögren-associated non-Hodgkin lymphomas and is regulated by IL-18.

2015

Summary The aim of this study was to elucidate more clearly the role of interleukin (IL)-18 in modulating the IL-22 pathway in primary Sjögren's syndrome (pSS) patients and in pSS-associated lymphomas. Minor salivary glands (MSGs) from patients with pSS and non-specific chronic sialoadenitis (nSCS), parotid glands biopsies from non-Hodgkin lymphomas (NHL) developed in pSS patients, were evaluated for IL-18, IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and signal transducer and activator of transcription-3 (STAT-3) expression. MSGs IL-22R1-expressing cells were characterized by confocal microscopy and flow cytometry in pSS, nSCS and healthy controls. The effect of recom…

MaleSalivary Glandslaw.inventionInterleukin 22lawIL-22Immunology and AllergyMyeloid CellsIL-22R1Receptormedicine.diagnostic_testnon-Hodgkin lymphomaLymphoma Non-HodgkinInterleukin-17TranslationalInterleukin-18Lacrimal ApparatusInterleukinMiddle AgedHaematopoiesisSjogren's SyndromeIL-22BPRecombinant DNASjögren's syndromeInterleukin 18FemaleIL-18Signal TransductionAdultSTAT3 Transcription FactorImmunologyPrimary Cell CultureBiologyPeripheral blood mononuclear cellIL-18; IL-22; IL-22BP; IL-22R1; Sjögren's syndrome; non-Hodgkin lymphomaSialadenitisFlow cytometrystomatognathic systemmedicineHumansAgedInterleukinsMacrophagesReceptors InterleukinSettore MED/16 - Reumatologiastomatognathic diseasesGene Expression RegulationImmunologyLeukocytes MononuclearClinical and experimental immunology
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Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.

2014

Background Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal rol…

MessengerWistarProtein tyrosine phosphataseInbred C57BLBiochemistryOral and gastrointestinalSTAT3Mice2.1 Biological and endogenous factorsPhosphorylationAetiologySTAT3Non-Receptor Type 2CeruletideCancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 2Pancreatitis Acute NecrotizingNF-kappa B3. Good healthAcute NecrotizingAmylasesTumor necrosis factor alphaTCPTPCell activationCeruletideSTAT3 Transcription Factormedicine.medical_specialtyBiochemistry & Molecular BiologyKnockoutBiologyProinflammatory cytokinePancreatic CancerRare DiseasesInternal medicineAcinar cellmedicineGeneticsAnimalsRNA MessengerRats WistarMolecular BiologyInflammationTumor Necrosis Factor-alphaInterleukin-6ResearchCell BiologyLipaseNFKB1RatsAcute pancreatitisMice Inbred C57BLEndocrinologyPancreatitisbiology.proteinRNAProtein Tyrosine PhosphataseBiochemistry and Cell BiologyDigestive DiseasesKnockout mice
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Activated IL-22 pathway occurs in the muscle tissues of patients with polymyositis or dermatomyositis and is correlated with disease activity.

2014

OBJECTIVE: The aim of this study was to assess the expression of IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and p-STAT3 in muscle tissue from patients with PM and DM. METHODS: Levels of IL-22, IL-22R1, IL-22BP and STAT3 mRNA were quantified by RT-PCR. The expression of IL-22, IL-22R1, IL-22BP and p-STAT3 was also analysed using immunohistochemistry. RESULTS: Significant modulation of the IL-22 pathway was observed in inflammatory myopathic tissues. In particular, a significant overexpression of IL-22 at the protein but not the mRNA level was observed in PM/DM tissues and was correlated with myositis activity. IL-22R1 aberrant expression was also observed among infilt…

Muscle tissueSTAT3 Transcription FactorPathologymedicine.medical_specialtyBiopsyPolymyositisSeverity of Illness IndexDermatomyositisInterleukin 22NecrosisRheumatologySettore BIO/13 - Biologia ApplicataMedicineMyocyteHumansPharmacology (medical)RNA MessengerReceptorMuscle SkeletalPolymyositiInflammationbusiness.industrySettore MED/27 - NeurochirurgiaInterleukinsReceptors InterleukinDermatomyositismedicine.diseasePolymyositisSettore MED/16 - Reumatologiamedicine.anatomical_structureInterleukin 22Case-Control StudiesImmunohistochemistryInterleukin 17businessSignal Transduction
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Fragmentation in the ϕ3 theory and the LPHD hypothesis

2015

We present analytic solution of the Dokshitzer-Gribov-Lipatov-Altarelli-Parisi (DGLAP) equation at leading order (LO) in the phi^3 theory in 6 space-time dimensions. If the phi^3 model was the theory of strong interactions, the obtained solution would describe the distribution of partons in a jet. We point out that the local parton-hadron duality (LPHD) conjecture does not work in this hypothetical situation. That is, treatment of hadronisation of shower partons is essential for the description of hadron distributions in jets stemming from proton-proton (pp) collisions at \sqrt{s} = 7 TeV and from electron-positron (e+e-) annihilations at various collision energies. We use a statistical mod…

Nuclear and High Energy PhysicsParticle physicsHadronFOS: Physical sciencesParton01 natural sciencesHigh Energy Physics - Phenomenology (hep-ph)Fragmentation (mass spectrometry)0103 physical sciencesNuclear Experiment010306 general physicsquantum field theoryPhysicsConjectureta114local parton-hadron duality010308 nuclear & particles physicsHigh Energy Physics::PhenomenologyAstronomy and AstrophysicsStatistical modelCollisionAtomic and Molecular Physics and OpticsHadronizationHigh Energy Physics - PhenomenologyDGLAPHigh Energy Physics::Experimentphi^3 theoryhadronizationInternational Journal of Modern Physics A
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IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease

2011

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production…

PathologyPulmonologymedicine.medical_treatmentT-LymphocytesIntracellular Spacelcsh:Medicine10263 Institute of Experimental ImmunologyInterleukin 22Mice0302 clinical medicineLymphocytesPhosphorylationlcsh:ScienceLung0303 health sciencesMultidisciplinaryInterleukin-13T CellsAllergy and HypersensitivityInnate lymphoid cellInterleukinrespiratory systemInnate ImmunityRecombinant Proteins3. Good healthCytokinemedicine.anatomical_structureInterleukin 13CytokinesMedicineTumor necrosis factor alphaBiological Markersmedicine.symptomResearch ArticleSTAT3 Transcription Factormedicine.medical_specialtyImmune CellsImmunologyAntigen-Presenting CellsImmunoglobulinsInflammation610 Medicine & health1100 General Agricultural and Biological SciencesBiology03 medical and health sciences1300 General Biochemistry Genetics and Molecular BiologymedicineRespiratory HypersensitivityAnimalsBiology030304 developmental biologyInflammation1000 MultidisciplinaryTumor Necrosis Factor-alphaInterleukinslcsh:RImmunityEpithelial CellsEosinophilAllergensAsthmaImmunity Innaterespiratory tract diseasesImmune SystemImmunology570 Life sciences; biologylcsh:QImmunizationBiomarkers030215 immunology
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Protective effect of apocynin in a mouse model of chemically-induced colitis.

2013

Apocynin, a constituent of Picrorhiza kurroa, successfully inhibits NADPH oxidase and shows promise as an anti-inflammatory drug. Now, we report anti-inflammatory effects of apocynin in an experimental colitis model induced by dextran sulfate sodium as well as the effects on the mediators involved in this process. Apocynin reduced the colitis induced in mice by administration of 5 % dextran sulfate sodium during 7 days. Mice were fed a control diet or a diet supplemented with 2 % of apocynin or 2 % of rutin. Sulfasalazine (50 mg/kg, p. o.) was used as a positive control. Treatment with apocynin and rutin ameliorated the course of colonic inflammation with results similar to those of the ref…

Picrorhiza kurroaRutinAnti-Inflammatory AgentsPharmaceutical ScienceNitric Oxide Synthase Type IIPharmacologyInflammatory bowel diseaseAnalytical Chemistrychemistry.chemical_compoundRutinMiceDrug DiscoveryPicrorhizaNADPH oxidasebiologyDextran SulfateColitisBiochemistrycardiovascular systemMolecular Medicinecirculatory and respiratory physiologymedicine.druginorganic chemicalsSTAT3 Transcription FactorColonNitric OxideDinoprostoneNitric oxideSulfasalazinemedicineAnimalscardiovascular diseasesColitisPharmacologyCyclooxygenase 2 Inhibitorsbusiness.industryPlant ExtractsOrganic ChemistryTranscription Factor RelAAcetophenonesmedicine.diseaseSulfasalazineDisease Models AnimalchemistryComplementary and alternative medicineCyclooxygenase 2Apocyninbiology.proteinbusinessPhytotherapyPlanta medica
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Cyclic AMP-induced Chromatin Changes Support the NFATc-mediated Recruitment of GATA-3 to the Interleukin 5 Promoter

2008

Elevated intracellular cyclic AMP levels, which suppress the proliferation of naive T cells and type 1 T helper (Th1) cells are a property of T helper 2 (Th2) cells and regulatory T cells. While cyclic AMP signals interfere with the IL-2 promoter induction, they support the induction of Th2-type genes, in particular of il-5 gene. We show here that cyclic AMP signals support the generation of three inducible DNase I hypersensitive chromatin sites over the il-5 locus, including its promoter region. In addition, cyclic AMP signals enhance histone H3 acetylation at the IL-5 promoter and the concerted binding of GATA-3 and NFATc to the promoter. This is facilitated by direct protein-protein inte…

Quantitative Trait LociGATA3 Transcription FactorBiologyBiochemistryCell LineHistonesMiceTh2 CellsCyclic AMPTranscriptional regulationAnimalsHumansTranscription Chromatin and EpigeneticsPromoter Regions GeneticHistone H3 acetylationMolecular BiologyInterleukin 5Cell ProliferationMice Inbred BALB CNFATC Transcription FactorsEffectorLymphokineAcetylationZinc FingersPromoterCell BiologyDNA-binding domainTh1 CellsChromatin Assembly and DisassemblyMolecular biologyChromatinProtein Structure TertiaryChromatinGene Expression RegulationInterleukin-2Interleukin-5Signal TransductionJournal of Biological Chemistry
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