Search results for "interleukin-17"

showing 10 items of 110 documents

IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice

2009

The clear association of Th17 cells with autoimmune pathogenicity implicates Th17 cytokines as critical mediators of chronic autoimmune diseases such as EAE. To study the impact of IL-17A on CNS inflammation, we generated transgenic mice in which high levels of expression of IL-17A could be initiated after Cre-mediated recombination. Although ubiquitous overexpression of IL-17A led to skin inflammation and granulocytosis, T cell–specific IL-17A overexpression did not have a perceptible impact on the development and health of the mice. In the context of EAE, neither the T cell–driven overexpression of IL-17A nor its complete loss had a major impact on the development of clinical disease. Sin…

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentT cellEncephalomyelitisPopulation610 Medicine & healthMice TransgenicInflammation2700 General Medicine10263 Institute of Experimental ImmunologyMyelin oligodendrocyte glycoproteinMicemedicineAnimalseducationCells CulturedGlycoproteinseducation.field_of_studybiologybusiness.industryInterleukin-17General MedicineTh1 Cellsmedicine.diseasePeptide FragmentsMice Inbred C57BLCytokinemedicine.anatomical_structureImmunologybiology.protein570 Life sciences; biologyExperimental pathologyFemaleMyelin-Oligodendrocyte GlycoproteinInterleukin 17medicine.symptombusinessGranulocytesResearch Article
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Imiquimod-Induced Psoriasis in Mice Depends on the IL-17 Signaling of Keratinocytes

2018

The pathology of psoriasis strongly depends on IL-17A. Monoclonal antibodies blocking either the cytokine or its receptor are among the most efficient treatments for psoriatic patients. Keratinocytes can be activated upon exposure to IL-17A and tumor necrosis factor-α and secrete secondary cytokines and chemokines in the inflamed skin. In psoriasis and its imiquimod-induced mouse model, a strong skin infiltration of neutrophils and inflammatory monocytes can be observed. However, to date, it is not clear how exactly those cellular populations are attracted to the skin and how they contribute to the pathogenesis of the disease. To define the crucial cell type responding to IL-17 and initiati…

KeratinocytesMale0301 basic medicineCell typeChemokinemedicine.medical_treatmentImiquimodDermatologyReal-Time Polymerase Chain ReactionBiochemistryMiceRandom Allocation03 medical and health sciences0302 clinical medicineAdjuvants ImmunologicPsoriasismedicineAnimalsPsoriasisMolecular BiologyCells CulturedImiquimodbiologyTumor Necrosis Factor-alphabusiness.industryBiopsy NeedleInterleukin-17Cell BiologyFlow Cytometrymedicine.diseaseImmunohistochemistryMice Inbred C57BLDisease Models Animal030104 developmental biologyCytokinemedicine.anatomical_structure030220 oncology & carcinogenesisImmunologybiology.proteinCytokinesFemaleTumor necrosis factor alphaInterleukin 17KeratinocytebusinessSignal Transductionmedicine.drugJournal of Investigative Dermatology
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Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation

2018

The chronic skin inflammation psoriasis is crucially dependent on the IL-23/IL-17 cytokine axis. Although IL-23 is expressed by psoriatic keratinocytes and immune cells, only the immune cell-derived IL-23 is believed to be disease relevant. Here we use a genetic mouse model to show that keratinocyte-produced IL-23 is sufficient to cause a chronic skin inflammation with an IL-17 profile. Furthermore, we reveal a cell-autonomous nuclear function for the actin polymerizing molecule N-WASP, which controls IL-23 expression in keratinocytes by regulating the degradation of the histone methyltransferases G9a and GLP, and H3K9 dimethylation of the IL-23 promoter. This mechanism mediates the inducti…

KeratinocytesMale0301 basic medicinemedicine.medical_treatmentWiskott-Aldrich Syndrome Protein NeuronalGeneral Physics and AstronomyEpigenesis GeneticHistonesMice0302 clinical medicineGenes ReporterInterleukin 23Promoter Regions Geneticlcsh:ScienceSkinMice KnockoutMultidisciplinaryInterleukin-17QMiddle AgedCytokine030220 oncology & carcinogenesisHistone methyltransferaseTumor necrosis factor alphaSignal transductionmedicine.symptomSignal TransductionAdultScienceGreen Fluorescent ProteinsPrimary Cell CultureInflammationBiologyArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesImmune systemPsoriasismedicineAnimalsHumansPsoriasisInflammationHistone-Lysine N-MethyltransferaseGeneral Chemistrybiochemical phenomena metabolism and nutritionmedicine.diseaseDisease Models AnimalHEK293 Cells030104 developmental biologyInterleukin-23 Subunit p19Cancer researchlcsh:QNature Communications
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Ciona intestinalis interleukin 17-like genes expression is upregulated by LPS challenge

2015

In humans, IL-17 is a proinflammatory cytokine that plays a key role in the clearance of extracellular bacteria promoting cell infiltration and production of several cytokines and chemokines. Here, we report on three Ciona intestinalis IL-17 homologues (CiIL17-1, CiIL17-2, CiIL17-3). The gene organisation, phylogenetic tree and modelling supported the close relationship with the mammalian IL-17A and IL-17F suggesting that the C. intestinalis IL-17 genes share a common ancestor in the chordate lineages. Real time PCR analysis showed a prompt expression induced by LPS inoculation suggesting that they are involved in the first phase of inflammatory response. In situ hybridization assays disclo…

LipopolysaccharidesChemokineLPSHemocytesAscidianMolecular Sequence DataImmunologySettore BIO/05 - ZoologiaIn situ hybridizationBiologyGranulocyteProinflammatory cytokineExtracellularmedicineAnimalsHumansProtein IsoformsCiona intestinalisAmino Acid SequenceGenePhylogenyInflammationBase SequenceInterleukin-17InterleukinSequence Analysis DNAbiology.organism_classificationCiona intestinalisCell biologyinterleukin IL17 hemocytemedicine.anatomical_structureImmunologybiology.proteinAscidian; interleukin IL17 hemocyte; inflammation; LPS; Ciona intestinalisSequence AlignmentDevelopmental Biology
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The nuclear receptor PPARγ selectively inhibits Th17 differentiation in a T cell–intrinsic fashion and suppresses CNS autoimmunity

2009

T helper cells secreting interleukin (IL)-17 (Th17 cells) play a crucial role in autoimmune diseases like multiple sclerosis (MS). Th17 differentiation, which is induced by a combination of transforming growth factor (TGF)-beta/IL-6 or IL-21, requires expression of the transcription factor retinoic acid receptor-related orphan receptor gamma t (ROR gamma t). We identify the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR gamma) as a key negative regulator of human and mouse Th17 differentiation. PPAR gamma activation in CD4(+) T cells selectively suppressed Th17 differentiation, but not differentiation into Th1, Th2, or regulatory T cells. Control of Th17 differentia…

MESH: Nuclear Receptor Subfamily 1 Group F Member 3Helper-InducerReceptors Retinoic AcidT-LymphocytesMESH: Interleukin-17Cellular differentiationRetinoic AcidPeroxisome proliferator-activated receptorNeurodegenerativeInbred C57BLMedical and Health SciencesMiceInterleukin 210302 clinical medicineGroup FRAR-related orphan receptor gammaMESH: Nuclear Receptor Co-Repressor 2Receptors2.1 Biological and endogenous factorsThyroid HormoneImmunology and AllergyMESH: AnimalsAetiologyEncephalomyelitisPromoter Regions Geneticchemistry.chemical_classificationOrphan receptor0303 health sciencesReceptors Thyroid HormoneInterleukin-17Cell DifferentiationT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 33. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureMESH: Repressor Proteins[SDV.IMM]Life Sciences [q-bio]/ImmunologyInterleukin 17MESH: Cell Differentiationmedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisNuclear Receptor Subfamily 1Member 31.1 Normal biological development and functioningT cellImmunologyBiologyAutoimmune DiseasePromoter RegionsExperimental03 medical and health sciencesGeneticUnderpinning researchMESH: Mice Inbred C57BLInternal medicineMESH: Promoter Regions GeneticGeneticsmedicineAnimalsHumansNuclear Receptor Co-Repressor 2MESH: Receptors Thyroid HormoneMESH: T-Lymphocytes Helper-InducerMESH: Encephalomyelitis Autoimmune ExperimentalMESH: Mice030304 developmental biologyMESH: Receptors Retinoic AcidMESH: HumansInflammatory and immune systemNeurosciencesBrief Definitive ReportCorrectionMESH: Multiple SclerosisBrain DisordersMice Inbred C57BLPPAR gammaRepressor ProteinsEndocrinologyMESH: PPAR gammaNuclear receptorchemistryMESH: DNA-Binding Proteins030217 neurology & neurosurgeryAutoimmuneJournal of Experimental Medicine
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Tuft cell‐derived IL‐25 activates and maintains ILC2

2016

Parasitic helminths and allergens induce a type 2 immune response leading to profound changes in tissue physiology, including hyperplasia of mucus-secreting goblet cells1 and smooth muscle hypercontractility2. This response, known as ‘weep and sweep’, requires interleukin (IL)-13 production by tissue-resident group 2 innate lymphoid cells (ILC2s) and recruited type 2 helper T cells (TH2 cells)3. Experiments in mice and humans have demonstrated requirements for the epithelial cytokines IL-33, thymic stromal lymphopoietin (TSLP) and IL-25 in the activation of ILC2s4–11, but the sources and regulation of these signals remain poorly defined. In the small intestine, the epithelium consists of at…

Male0301 basic medicineAllergyImmunologyInnate immunologyBiologyArticle03 medical and health sciences0302 clinical medicineImmune systemIntestinal mucosaImmunitymedicineAnimalsImmunology and AllergyLymphocytesIntestinal MucosaImmunity MucosalInterleukin-17Cell Biologymedicine.diseaseImmunity Innate030104 developmental biologyMucosal immunologyImmunologyFemaleInterleukin 17Tuft cell030215 immunologyImmunology & Cell Biology
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Interleukin-17 Inhibition in Spondyloarthritis Is Associated With Subclinical Gut Microbiome Perturbations and a Distinctive Interleukin-25-Driven In…

2020

Objective To characterize the ecological effects of biologic therapies on the gut bacterial and fungal microbiome in psoriatic arthritis (PsA)/spondyloarthritis (SpA) patients. Methods Fecal samples from PsA/SpA patients pre- and posttreatment with tumor necrosis factor inhibitors (TNFi; n = 15) or an anti-interleukin-17A monoclonal antibody inhibitor (IL-17i; n = 14) underwent sequencing (16S ribosomal RNA, internal transcribed spacer and shotgun metagenomics) and computational microbiome analysis. Fecal levels of fatty acid metabolites and cytokines/proteins implicated in PsA/SpA pathogenesis or intestinal inflammation were correlated with sequence data. Additionally, ileal biopsies obtai…

Male0301 basic medicineArthritisPsoriatic0302 clinical medicineInterleukin 25Monoclonal2.1 Biological and endogenous factorsImmunology and AllergyMedicineAetiologyIntestinal MucosaCandida albicansHumanizedSubclinical infectionbiologyInterleukin-17Innate lymphoid cellMiddle AgedIntestinesPublic Health and Health ServicesFemaleTumor necrosis factor alphaInterleukin 17Clinical SciencesImmunologyAntibodies Monoclonal HumanizedAutoimmune DiseaseAntibodiesArticle03 medical and health sciencesRheumatologyClinical ResearchSpondylarthritisHumansMicrobiomeInflammation030203 arthritis & rheumatologybusiness.industryArthritisInflammatory and immune systemArthritis Psoriaticbiology.organism_classificationmedicine.diseaseArthritis & RheumatologyGastrointestinal Microbiome030104 developmental biologyImmunologyTumor Necrosis Factor InhibitorsDigestive Diseasesbusiness
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Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma

2016

Obesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of t…

Male0301 basic medicineCancer ResearchCarcinoma HepatocellularInflammationWhite adipose tissueDiet High-FatMice03 medical and health sciencesNon-alcoholic Fatty Liver DiseasemedicineAnimalsHumansUnconventional prefoldin RPB5 interactorbiologyInterleukin-17Liver NeoplasmsFatty liverIntracellular Signaling Peptides and ProteinsCell Biologymedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyNeutrophil InfiltrationOncologyHepatocellular carcinomaImmunologybiology.proteinTh17 CellsInterleukin 17SteatosisSteatohepatitismedicine.symptomDNA DamageCancer Cell
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The complex alteration in the network of IL-17-type cytokines in patients with hereditary angioedema

2018

Hereditary angioedema (HAE) is a rare autosomic-dominant disorder characterized by a deficiency of C1 esterase inhibitor which causes episodic swellings of subcutaneous tissues, bowel walls and upper airways that are disabling and potentially life-threatening. We evaluated n = 17 patients with confirmed HAE diagnosis during attack and remission state and n = 19 healthy subjects. The samples were tested for a panel of IL (Interleukin)-17-type cytokines (IL-1β, IL-6, IL-10, granulocyte–macrophage colony stimulating factor (GM-CSF), IL-17, IL-21, IL-22, IL-23) and transforming growth factor-beta (TGF-β) subtypes. Data indicate that there are variations of cytokine levels in HAE subjects compar…

Male0301 basic medicinemedicine.medical_treatmentC1 esterase inhibitorInterleukin-23chemistry.chemical_compoundSubcutaneous TissueTransforming Growth Factor betaChildHereditary angioedemaHematologyInterleukin-17InterleukinGeneral MedicineMiddle AgedIntestinesCytokineHereditary angioedemaFemaleInterleukin 17medicine.symptomComplement C1 Inhibitor ProteinAdultmedicine.medical_specialtyAdolescentBradykininBronchiBradykininGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInternal medicinemedicineHumansCytokineAgedBiochemistry Genetics and Molecular Biology (all)Angioedemabusiness.industryInterleukinsAngioedemas HereditaryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseColony-stimulating factor030104 developmental biologyGene Expression RegulationchemistryCase-Control StudiesImmunologyTh17 CellsbusinessClinical and Experimental Medicine
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Oral Palmitoylethanolamide Treatment Is Associated with Reduced Cutaneous Adverse Effects of Interferon-β1a and Circulating Proinflammatory Cytokines…

2016

Palmitoylethanolamide (PEA) is an endogenous lipid mediator known to reduce pain and inflammation. However, only limited clinical studies have evaluated the effects of PEA in neuroinflammatory and neurodegenerative diseases. Multiple sclerosis (MS) is a chronic autoimmune and inflammatory disease of the central nervous system. Although subcutaneous administration of interferon (IFN)-β1a is approved as first-line therapy for the treatment of relapsing–remitting MS (RR-MS), its commonly reported adverse events (AEs) such as pain, myalgia, and erythema at the injection site, deeply affect the quality of life (QoL) of patients with MS. In this randomized, double-blind, placebo-controlled study,…

Male0301 basic medicinemyalgiaErythemaAnti-Inflammatory AgentsPalmitic AcidAdministration OralPharmacologyGastroenterologychemistry.chemical_compound0302 clinical medicineNeuroinflammationFAAHEthanolaminePharmacology (medical)SkinInterleukin-17food and beveragesAnti-Inflammatory AgentTolerabilityEthanolaminesDisease ProgressionCytokinesOriginal ArticleFemalemedicine.symptomInterferon beta-1aHumanAdultmedicine.medical_specialtyPainPalmitic AcidsProinflammatory cytokineInterferon-gamma03 medical and health sciencesMultiple Sclerosis Relapsing-RemittingDouble-Blind MethodInternal medicinemedicineHumansAdverse effectCytokinePharmacologyPalmitoylethanolamideExpanded Disability Status ScaleTumor Necrosis Factor-alphabusiness.industryMultiple sclerosisN-acylethanolamineOleoylethanolamideAnandamideNAAAmedicine.diseaseAmides030104 developmental biologychemistryNeurology (clinical)business030217 neurology & neurosurgeryNeurotherapeutics
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