Search results for "STAT3"

showing 10 items of 106 documents

Rituximab modulates IL-17 expression in the salivary glands of patients with primary Sjögren's syndrome.

2014

OBJECTIVE: The aim of this study was to evaluate the role of rituximab (RTX) in modulating the expression of the IL-17/IL-23 pathway in the salivary glands (SGs) of patients with primary SS (pSS). METHODS: Consecutive SG biopsies were obtained from 15 patients with pSS before and after 1 year of RTX therapy. The SG expression of IL-17, IL-23p19 and p-STAT3 was evaluated by immunohistochemistry at baseline and after RTX therapy. The role of mast cells in pSS patients in modulating the Th17 response and the immunologic effect of RTX on mast cells were also studied in in vitro experiments. RESULTS: IL-17 was overexpressed in the SGs of patients with pSS mainly by infiltrating T cells and mast …

AdultMaleSTAT3 Transcription FactorSjogren SyndromeApoptosisIn Vitro TechniquesInterleukin-23Peripheral blood mononuclear cellSalivary GlandsAntibodies Monoclonal Murine-DerivedRheumatologystomatognathic systemSettore BIO/13 - Biologia ApplicataBiopsyHumansMedicinePharmacology (medical)Mast CellsAgedmedicine.diagnostic_testbusiness.industryInterleukinsInterleukin-17IL17Middle AgedMast cellIn vitroSettore MED/16 - ReumatologiaSjogren's SyndromeTreatment Outcomemedicine.anatomical_structureApoptosisAntirheumatic AgentsImmunologyTh17 CellsImmunohistochemistryFemaleRituximabInterferonsInterleukin 17businessRituximabSignal Transductionmedicine.drug
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Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation: Evidence in Crohn diseas…

2000

The pro-inflammatory cytokine interleukin (IL)-6 (refs. 1-5) can bind to cells lacking the IL-6 receptor (IL-6R) when it forms a complex with the soluble IL-6R (sIL-6R) (trans signaling). Here, we have assessed the contribution of this system to the increased resistance of mucosal T cells against apoptosis in Crohn disease (CD), a chronic inflammatory disease of the gastrointestinal tract. A neutralizing antibody against IL-6R suppressed established experimental colitis in various animal models of CD mediated by type 1 T-helper cells, by inducing apoptosis of lamina propria T cells. Similarly, specific neutralization of sIL-6R in vivo by a newly designed gp130-Fc fusion protein caused suppr…

AdultMaleSTAT3 Transcription FactorT-Lymphocytesmedicine.medical_treatmentT cellbcl-X ProteinApoptosisGeneral Biochemistry Genetics and Molecular BiologyMiceCrohn DiseaseAntigenAntigens CDCytokine Receptor gp130medicineAnimalsHumansInterleukin 6Mice Inbred BALB CMembrane GlycoproteinsbiologyInterleukin-6Models ImmunologicalInterleukinGeneral MedicineMiddle AgedReceptors Interleukin-6DNA-Binding ProteinsCytokinemedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisImmunologyTrans-Activatorsbiology.proteinSTAT proteinCancer researchColitis UlcerativeFemaleSignal transductionProtein BindingSignal TransductionNature Medicine
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Inhibition of miR-21 restores RANKL/OPG ratio in multiple myeloma-derived bone marrow stromal cells and impairs the resorbing activity of mature oste…

2015

// Maria Rita Pitari 1 , Marco Rossi 1 , Nicola Amodio 1 , Cirino Botta 1 , Eugenio Morelli 1 , Cinzia Federico 1 , Annamaria Gulla 1 , Daniele Caracciolo 1 , Maria Teresa Di Martino 1 , Mariamena Arbitrio 2 , Antonio Giordano 3, 4 , Pierosandro Tagliaferri 1 , Pierfrancesco Tassone 1, 4 1 Department of Experimental and Clinical Medicine and T. Campanella Cancer Center, Magna Graecia University, S. Venuta University Campus, Catanzaro, Italy 2 ISN-CNR, Roccelletta di Borgia, Catanzaro, Italy 3 Department of Human Pathology and Oncology, University of Siena, Siena, Italy 4 Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology,…

Bone diseaseMessengerOsteoclastsTumor Microenvironment3' Untranslated RegionsMultiple myelomaTumorbiologyMesenchymal Stromal CellsRANKLProtein Inhibitors of Activated STATUp-Regulationmedicine.anatomical_structureOncologyRANKLmiRNAsmiR-21MiRNAMultiple MyelomaMiR-21; MiRNAs; Multiple myeloma bone disease; OPG; RANKL; 3' Untranslated Regions; Bone Marrow Cells; Bone Resorption; Cell Adhesion; Cell Line Tumor; Coculture Techniques; HEK293 Cells; Humans; Interleukin-6; Lentivirus; Mesenchymal Stromal Cells; MicroRNAs; Molecular Chaperones; Multiple Myeloma; Osteoclasts; Osteoprotegerin; Protein Inhibitors of Activated STAT; RANK Ligand; RNA Messenger; STAT3 Transcription Factor; Stromal Cells; Tumor Microenvironment; Up-Regulation; OncologyResearch Papermusculoskeletal diseasesSTAT3 Transcription FactorStromal cellBone Marrow CellsBone resorptionCell LineOsteoprotegerinCell Line TumormedicineCell AdhesionHumansRNA MessengerBone Resorptionbusiness.industryInterleukin-6LentivirusRANK LigandOsteoprotegerinMesenchymal Stem Cellsmedicine.diseaseMolecular medicineCoculture TechniquesMicroRNAsmultiple myeloma bone diseaseHEK293 CellsImmunologyCancer researchbiology.proteinRNAOPGBone marrowStromal CellsbusinessMolecular ChaperonesOncotarget
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A new model of chronic colitis in SCID mice induced by adoptive transfer of CD62L+ CD4+ T cells: insights into the regulatory role of interleukin-6 o…

2003

<i>Objective:</i> The proinflammatory cytokine interleukin (IL)-6 is involved in various chronic inflammatory processes. IL-6 is a predominant cytokine produced by lamina propria T cells in Crohn’s disease and experimental colitis. This study was designed to examine the effect of a neutralizing IL-6-receptor (IL-6R) antibody on the programmed cell death of mucosal T cells in the CD62L+ CD4+ SCID transfer model of chronic experimental colitis in mice and to gain more insight into the pathogenesis of this transfer colitis model. <i>Methods:</i> For adoptive transfer, we isolated CD62L+ CD4+ double-positive T cells from wild-type BALB/c mice followed by intraperitoneal …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorAdoptive cell transferCell TransplantationColonApoptosisMice SCIDPathology and Forensic MedicineProinflammatory cytokineInterleukin 21MiceInterleukin 25In Situ Nick-End LabelingAnimalsIL-2 receptorIntestinal MucosaL-SelectinInterleukin 6Antibodies BlockingMolecular BiologyMice Inbred BALB CbiologyInterleukin-6InterleukinCell BiologyGeneral MedicineFlow CytometryAdoptive TransferReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalImmunologybiology.proteinTrans-ActivatorsInterleukin 18Colitis UlcerativeSevere Combined ImmunodeficiencySpleenPathobiology : journal of immunopathology, molecular and cellular biology
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Activation pattern of signal transducers and activators of transcription (STAT) factors in inflammatory bowel diseases.

2005

Cytokine signaling pathways involving transcription factors of the signal transducers and activators of transcription (STAT) family play a key role in the pathogenesis of inflammatory bowel diseases (IBD). STAT proteins are latent cytoplasmic transcription factors that induce transcription upon phosphorylation, dimerization, and nuclear translocation. However, their activation pattern in IBD is poorly understood. The aim of our study was to characterize STAT-expression in IBD.Mononuclear cells were isolated from 36 colonic specimens of Crohn's disease, ulcerative colitis, or from control patients. Cells were stimulated overnight with antibodies against human CD2 and CD28 and mononuclear cel…

CD4-Positive T-LymphocytesSTAT3 Transcription FactorColonActivation patternstatTranscription (biology)MedicineHumansSTAT4Transcription factorHepatologybusiness.industryActivator (genetics)digestive oral and skin physiologyGastroenterologySTAT2 Transcription FactorSTAT3 Transcription FactorSTAT4 Transcription FactorInflammatory Bowel Diseasesdigestive system diseasesDNA-Binding ProteinsSTAT1 Transcription FactorCase-Control StudiesImmunologyCancer researchTrans-ActivatorsSignal transductionbusinessSTAT6 Transcription FactorThe American journal of gastroenterology
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Local blockade of IL-6R signaling induces lung CD4+ T cell apoptosis in a murine model of asthma via regulatory T cells.

2007

We previously reported high levels of the soluble form of the IL-6R (sIL-6R) in the airways of asthmatic subjects. Here, we analyzed the IL-6R effects on Th2 cell survival in the lung by locally antagonizing sIL-6R-mediated trans-signaling with a designer fusion protein (gp130-Fc) as well as IL-6R signaling with an antibody against the gp80 unit of the IL-6R (alphaIL-6R) in a murine model of asthma after ovalbumin peptide (OVA) sensitization and challenge. Blockade of the sIL-6R led to a significant decrease in inflammatory cells by an apoptosis-independent mechanism. In contrast, local treatment with alphaIL-6R antibodies that also block signaling via the membrane-bound IL-6R (mIL-6R) led …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorOvalbuminT cellRecombinant Fusion ProteinsImmunologyGene ExpressionApoptosisBiologyT-Lymphocytes RegulatoryAntibodiesInterleukin 21MicemedicineCytokine Receptor gp130Immunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPhosphorylationLungMice Inbred BALB CInterleukin-6FOXP3Forkhead Transcription FactorsGeneral MedicineT lymphocyterespiratory systemReceptors Interleukin-6AsthmaCoculture TechniquesImmunoglobulin Fc FragmentsDisease Models Animalmedicine.anatomical_structureApoptosisImmunologyCancer researchFemaleImmunizationSignal transductionBronchoalveolar Lavage FluidSignal TransductionInternational immunology
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Cutting Edge: IL-6–Driven Immune Dysregulation Is Strictly Dependent on IL-6R α-Chain Expression

2020

Abstract IL-6 binds to the IL-6R α-chain (IL-6Rα) and signals via the signal transducer gp130. Recently, IL-6 was found to also bind to the cell surface glycoprotein CD5, which would then engage gp130 in the absence of IL-6Rα. However, the biological relevance of this alternative pathway is under debate. In this study, we developed a mouse model, in which murine IL-6 is overexpressed in a CD11c-Cre–dependent manner. Transgenic mice developed a lethal immune dysregulation syndrome with increased numbers of Ly-6G+ neutrophils and Ly-6Chi monocytes/macrophages. IL-6 overexpression promoted activation of CD4+ T cells while suppressing CD5+ B-1a cell development. However, additional ablation of …

Genetically modified mouseImmunologyInflammationMice Transgenicmedicine.disease_cause03 medical and health sciencesMice0302 clinical medicineRare DiseasesmedicineImmunology and AllergyAnimals2.1 Biological and endogenous factorsInflammatory and Immune SystemReceptorSTAT3biologyCell growthChemistryInterleukin-6Immune dysregulationGlycoprotein 130Receptors Interleukin-6Cell biologybiology.proteinAlternative complement pathwaymedicine.symptom030215 immunologySignal TransductionThe Journal of Immunology
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TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling

2004

Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-depende…

Genetically modified mouseSTAT3 Transcription FactorColorectal cancerRecombinant Fusion ProteinsT-LymphocytesImmunologyBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicProtein Serine-Threonine KinasesMiceIn vivoTransforming Growth Factor betamedicineImmunology and AllergyAnimalsHumansEndoscopy Digestive SystemIntestinal MucosaInterleukin 6Autocrine signallingMice KnockoutbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionReceptor Transforming Growth Factor-beta Type IIHistologymedicine.diseaseImmunohistochemistryReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalInfectious DiseasesTumor progressionImmunologyColonic NeoplasmsCancer researchbiology.proteinDisease ProgressionTrans-ActivatorsReceptors Transforming Growth Factor betaTransforming growth factorSignal TransductionImmunity
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Induction of regulatory Tr1 cells and inhibition of TH17 cells by IL-27

2011

Accumulating evidence indicates that IL-27, a member of the IL-12 family of cytokines, alleviates the severity of autoimmune diseases in both mice and men. The IL-27-induced activation of signal transducer and activator of transcription (Stat)1 and Stat3 promotes the generation of IL-10- producing type 1 regulatory T (Tr1) cells that inhibit effector T cells. In addition, IL-27 also suppresses the development of pathogenic IL-17-producing CD4(+) T cells (T(H)17) cells suggesting that pharmacological manipulations of IL-27 signaling pathway could be exploited therapeutically in regulating tissue inflammation. Here, we review how IL-27 controls inflammation through the regulation of Tr1 and T…

Interleukins/immunologyImmunologyInterleukin-10/biosynthesis/immunologyT-Lymphocytes Regulatory/immunologyddc:616.07T-Lymphocytes RegulatoryArticleAutoimmune Diseases03 medical and health sciences0302 clinical medicineImmunology and AllergyCytotoxic T cellTh17 Cells/immunologyAnimalsHumansIL-2 receptorSTAT3STAT4030304 developmental biology0303 health sciencesbiologyZAP70InterleukinsFOXP33. Good healthCell biologyddc:616.8Interleukin-10Interleukin 10Autoimmune Diseases/immunologyImmunologyInterleukin 12biology.proteinTh17 Cells030215 immunology
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NF-κB and STAT3 Inhibition as a Therapeutic Strategy in Psoriasis: In Vitro and In Vivo Effects of BTH

2013

Benzo[b]thiophen-2-yl-3-bromo-5-hydroxy-5H-furan-2-one (BTH) is a simple and interesting synthetic derivative of petrosaspongiolide M, a natural compound isolated from a sea sponge with demonstrated potent anti-inflammatory activity through inhibition of the NF-κB signaling pathway. In the present study, we report the in vitro and in vivo pharmacological effect of BTH on some parameters related to the innate and adaptive response in the pathogenesis of psoriasis. BTH inhibited the release of some of the key psoriatic cytokines such as tumor necrosis factor α, IL-8, IL-6, and CCL27 through the downregulation of NF-κB in normal human keratinocytes. Moreover, it impaired signal transducers and…

KeratinocytesMaleSTAT3 Transcription FactorForeskinPrimary Cell CultureDermatitisInflammationDermatologyPharmacologyBiochemistryMicechemistry.chemical_compoundIn vivoPsoriasisThiadiazolesmedicineAnimalsHumansPsoriasisSTAT3Molecular BiologyCell ProliferationMice Inbred BALB CbiologyNF-kappa BNF-κBCell Biologymedicine.diseaseDisease Models Animalmedicine.anatomical_structurechemistrybiology.proteinCytokinesFemaleCCL27Signal transductionmedicine.symptomKeratinocyteJournal of Investigative Dermatology
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