Search results for "interleukin-17"

showing 10 items of 110 documents

IL-23 receptor regulates unconventional IL-17-producing T cells that control bacterial infections.

2010

AbstractIL-23 plays an important role in autoimmune tissue inflammation and induces the generation of not fully characterized effector cells that mediate protection against pathogens. In this paper, we established the essential role of IL-23R in the host response against intracellular pathogens. IL-23 was critical for the expansion or maintenance of γδ and double negative (DN) αβ T cells. These cells were rapidly recruited to the site of infection and produced large amounts of IL-17, IFN-γ, and TNF-α. Notably, DN T cells transferred into L. monocytogenes-infected RAG2−/− mice prevented bacterial growth, confirming their protective role against intracellular pathogens. Our results show that …

T cellCD8 AntigensReceptors Antigen T-Cell alpha-betaImmunologyMice NudeMice TransgenicBiologyArticleImmunophenotypingInterferon-gammaMiceImmune systemAntigenCell MovementT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsInterferon gammaListeriosisCells CulturedMice KnockoutEffectorTumor Necrosis Factor-alphaIntracellular parasiteInterleukin-17Receptors Antigen T-Cell gamma-deltaReceptors InterleukinCoculture TechniquesCell biologymedicine.anatomical_structureImmunologyCD4 AntigensInterleukin-23 Subunit p19Tumor necrosis factor alphaInterleukin 17Peritoneummedicine.drugJournal of immunology (Baltimore, Md. : 1950)
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New therapies for sepsis: focus on the interleukin (IL)12 family member IL27

2007

Sepsis is a severe complication of abdominal infections such as peritonitis and is associated with high mortality. Unfortunately, the molecular mechanisms controlling the development of sepsis are still incompletely understood. Interestingly, the interleukin (IL) 12 family member IL27 seems to play a key role in sepsis. In a murine model of septic peritonitis induced by caecal ligation and puncture (CLP), IL27 levels were found to be strongly induced. Furthermore, mice deficient for the EBI3 subunit of IL27 were resistant to CLP-induced septic peritonitis as compared to wild-type controls. This effect could be suppressed by injection of recombinant IL27. Further studies demonstrated that IL…

T-LymphocytesImmunologyPeritonitisPeritonitisGeneral Biochemistry Genetics and Molecular BiologySepsisMiceRheumatologySepsismedicineAnimalsHumansImmunology and AllergyInterleukin 27business.industryInterleukin-17InterleukinCell DifferentiationEBI3medicine.diseaseBlockadeDisease Models AnimalImmunologyInterleukin 12ImmunotherapyInterleukin 17Reactive Oxygen SpeciesbusinessSupplementAnnals of the Rheumatic Diseases
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Cutting Edge: A Key Pathogenic Role of IL-27 in T Cell- Mediated Hepatitis

2007

Abstract The signals driving T cell activation in T cell-mediated fulminant hepatitis are not fully understood. In this study, we identify the cytokine IL-27p28/EBI3 as a major pathogenic factor in the ConA model of T cell-mediated hepatitis. We found an up-regulation of hepatic EBI3 and p28 expression and augmented levels of IL-27 in wild-type mice after ConA administration, suggesting a potential pathogenic role of this cytokine in ConA hepatitis. Consistently, IL-27 EBI3-deficient mice were almost completely protected from ConA-induced liver damage. Such protection was associated with reduced levels of IFN-γ and its signaling proteins pSTAT-1 and T-bet. Finally, in vivo blockade of IL-27…

T-Lymphocytesmedicine.medical_treatmentT cellImmunologychemical and pharmacologic phenomenaBiologyMinor Histocompatibility AntigensInterferon-gammaMiceConcanavalin AmedicineAnimalsImmunology and AllergyReceptors CytokineReceptorFulminant hepatitisMice KnockoutHepatitisLiver injuryInterleukin-17EBI3medicine.diseaseUp-RegulationSTAT1 Transcription FactorCytokinemedicine.anatomical_structureImmunologyChemical and Drug Induced Liver InjurySignal transductionSignal TransductionThe Journal of Immunology
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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Beclomethasone dipropionate and formoterol reduce oxidative/nitrosative stress generated by cigarette smoke extracts and IL-17A in human bronchial ep…

2013

Interleukin-17A (IL-17A), cigarette smoke and oxidative/nitrosative stress are involved in inflammatory airway diseases, and the mechanisms behind these processes are still poorly understood. We investigated whether recombinant human IL-17A (rhIL-17A), in combination with cigarette smoke extracts (CSE), increases the levels of inducibile nitric oxide synthase (iNOS), reactive oxygen species, nitrotyrosine (NT) and the activation of signal transducer and activator of transcription 1 (STAT-1) in normal human bronchial epithelial cells (16HBE). The effect of beclomethasone dipropionate (BDP), formoterol and their combination was also evaluated. We demonstrated that rhIL-17A or CSE alone increa…

Transcription GeneticNitric Oxide Synthase Type IIBronchiOxidative phosphorylationPharmacologyGene Expression Regulation EnzymologicCell Linechemistry.chemical_compoundFormoterol FumarateSmokeNitrilesmedicineButadienesGene silencingHumansGene SilencingPromoter Regions GeneticPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyNitrotyrosineInterleukin-17BeclomethasoneEpithelial CellsTobacco ProductsReactive Nitrogen SpeciesNitric oxide synthaseOxidative StressSTAT1 Transcription FactorchemistryEthanolaminesImmunologySTAT proteinbiology.proteinPhosphorylationFormoterolBiomarkersmedicine.drugEuropean journal of pharmacology
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Pro-inflammatory effects of interleukin-17A on vascular smooth muscle cells involve NAD(P)H- oxidase derived reactive oxygen species.

2010

T cells are known for their contribution to the inflammatory element of atherosclerosis. Recently, it has been demonstrated that the Th17 derived cytokine IL-17 is involved in the pro-inflammatory response of vascular smooth muscle cells (VSMC). The aim of the present study was to examine whether reactive oxygen species (ROS) might be involved in this context. The effect of IL-17A on ROS generation was examined using the fluorescent dye 2′7′-dichlorodihydrofluorescein (H<sub>2</sub>DCF) in primary murine VSMC. IL-17A induced an increase in H<sub>2</sub>DCF fluorescence in VSMC, and this effect was blocked by the NAD(P)H-oxidase inhibitor apocynin and siRNA targeting …

Vascular smooth musclePhysiologymedicine.medical_treatmentAorta Thoracicmedicine.disease_causep38 Mitogen-Activated Protein KinasesMuscle Smooth Vascularchemistry.chemical_compoundMiceCell MovementmedicineAnimalsEnzyme InhibitorsRNA Small InterferingCells Culturedchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseMembrane GlycoproteinsbiologyInterleukin-17AcetophenonesNADPH OxidasesCell DifferentiationMolecular biologyMice Inbred C57BLOxidative StressCytokinechemistryBiochemistryNAD(P)H oxidaseNADPH Oxidase 4ApocyninNADPH Oxidase 2cardiovascular systembiology.proteinCytokinesNAD+ kinaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressJournal of vascular research
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Cutting Edge: An IL-17F-CreEYFP Reporter Mouse Allows Fate Mapping of Th17 Cells

2009

Abstract The need for reporter lines able to faithfully track Th17 cells in vivo has become an issue of exceptional importance. To address this, we generated a mouse strain in which Cre recombinase is expressed from the IL-17F promoter. Crossing the IL-17F-Cre allele to a conditional enhanced yellow fluorescent protein (EYFP) reporter mouse yielded the IL-17F-CreEYFP strain, in which IL-17F expression is twinned with EYFP in live IL-17F-expressing cells. Although we demonstrate that IL-17F expression is restricted to CD4+ T cells during experimental autoimmune encephalomyelitis, IL-17F-CreEYFP CD8 T cells robustly expressed IL-17F in response to TGF-β, IL-6, and IL-23. Fate mapping of IL-17…

Yellow fluorescent proteinAdoptive cell transferEncephalomyelitis Autoimmune ExperimentalRNA UntranslatedTransgeneImmunologyCre recombinaseMice TransgenicCD8-Positive T-LymphocytesT-Lymphocytes RegulatoryImmunophenotypingMiceBacterial ProteinsGenes ReporterFate mappingAnimalsHumansImmunology and AllergyCytotoxic T cellCells CulturedIntegrasesbiologyInterleukin-17ProteinsCell DifferentiationAdoptive TransferMolecular biologyPhenotypeIn vitroMice Inbred C57BLLuminescent ProteinsGene Expression RegulationMice Inbred DBAbiology.proteinThe Journal of Immunology
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Il-6 signaling in inflammatory bowel disease: pathophysiological role and clinical relevance.

2007

Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory bowel diseases (IBDs) occurring in the gut of genetically susceptible individuals independent of a specific pathogen. The interaction between antigen-presenting cells and the local bacterial flora contributes to an uncontrolled activation of mucosal CD4+ T lymphocytes with the consecutive release of proinflammatory cytokines such as tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, IL-23, IL-27, and also IL-17, which is attributed to a specific, differentiated CD4+ lineage called Th17 (TH-IL17, THi). Recent data suggest that IL-6 contributes to Th17 differentiation. However, to clarify the importance of Th17 cel…

biologyInterleukin-6Interleukin-17GastroenterologyInterleukinInflammationApoptosismedicine.diseaseInflammatory Bowel DiseasesInflammatory bowel diseaseReceptors Interleukin-6Proinflammatory cytokineInterleukin-6 receptorImmunologymedicinebiology.proteinImmunology and AllergyAnimalsHumansTumor necrosis factor alphaInterleukin 17medicine.symptomInterleukin 6Signal TransductionInflammatory bowel diseases
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Role of the IL-23/IL-17 Pathway in Rheumatic Diseases: An Overview

2021

Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, IL-23A (p19) and IL-12/23B (p40), the latter shared with Interleukin-12 (IL-12). IL-23 is mainly produced by macrophages and dendritic cells, in response to exogenous or endogenous signals, and drives the differentiation and activation of T helper 17 (Th17) cells with subsequent production of IL-17A, IL-17F, IL-6, IL-22, and tumor necrosis factor α (TNF-α). Although IL-23 plays a pivotal role in the protective immune response to bacterial and fungal infections, its dysregulation has been shown to exacerbate chronic immune-mediated inflammation. Well-established experimental data support the concept that IL-23/IL…

lcsh:Immunologic diseases. Allergy0301 basic medicinemedicine.medical_treatmentImmunologyinflammatory diseasesInflammationautoimmune diseaseAutoimmunityReviewInflammatory bowel diseaseInterleukin-23Th17 CellRheumatic Disease03 medical and health sciencesPsoriatic arthritis0302 clinical medicineImmune systemIL-23PsoriasisRheumatic DiseasesInterleukin 23medicineAnimalsHumansImmunology and Allergyautoimmune diseasesMolecular Targeted TherapyIL-23/IL-17 axi030203 arthritis & rheumatologyInflammationbusiness.industryIL-23/IL-17 axisAnimalInterleukin-17medicine.diseaseinflammatory diseaseIL-17030104 developmental biologyCytokineImmunologyTh17 CellsInterleukin 17medicine.symptomlcsh:RC581-607businessHuman
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A Case of Moderate Hidradenitis Suppurativa and Psoriasis Treated with Secukinumab

2018

Hidradenitis suppurativa (HS) is a disorder of the apocrine gland causing a chronic, recurrent and painful inflammation. It is a disabilitating condition and, though many therapeutic options are available, the response is often ineffective in most cases and patients can present many recurrences with physical and psychological sequelae. Recent data had shown increased interleukin (IL)-17 serum levels in patients with HS. Psoriasis is a chronic immune-mediated inflammatory disorder and new evidences have shown the role of Th17 cells in its pathogenesis and the therapeutic efficacy of anti-IL-17 antibodies. We present a case of a patient suffering from psoriasis and HS successfully treated wit…

medicine.medical_specialtybusiness.industryInterleukin-17ApocrineInterleukinCase ReportInflammationDermatologymedicine.diseaseDermatologyPathogenesisHidradenitis suppurativa030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicine030220 oncology & carcinogenesisPsoriasismedicinePsoriasisHidradenitis suppurativaSecukinumabInterleukin 17medicine.symptombusinessAnnals of Dermatology
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