Search results for "Interleukin 17"

showing 10 items of 75 documents

Protective role of nuclear factor of activated T cells 2 in CD8+ long-lived memory T cells in an allergy model

2007

Background The transcriptional regulation of cytokines released and controlled by memory T cells is not well understood. Defective IFN-γ production in allergic asthma correlates in human beings with the risk of wheezing in childhood. Objective To understand the role of the transcription factor nuclear factor of activated T cells 2 (NFATc2) in memory and effector T cells in the airways in experimental allergic asthma. Methods We used murine models of allergic asthma and adoptive cell transfer of fluorescence-activated sorted cells in a disease model. Results Mice lacking NFATc2 developed an increase in airway hyperresponsiveness (AHR), remodeling, and serum IgE levels on ovalbumin sensitizat…

MaleInterleukin 2Adoptive cell transferImmunologyMice SCIDCD8-Positive T-LymphocytesInterferon-gammaMiceInterleukin 21T-Lymphocyte SubsetsHypersensitivitymedicineAnimalsImmunology and AllergyCytotoxic T cellInterleukin-7 receptorLungMice KnockoutMice Inbred BALB CReceptors Interleukin-7NFATC Transcription Factorsbusiness.industryInterleukin-17Cell Differentiationrespiratory systemAdoptive TransferMolecular biologyGrowth InhibitorsUp-Regulationrespiratory tract diseasesInterleukin-2 Receptor beta SubunitInterleukin 10ImmunologyFemaleInterleukin 17Bronchial HyperreactivitybusinessImmunologic MemoryCD8medicine.drugJournal of Allergy and Clinical Immunology
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Expression of Interleukin-32 in the Inflamed Arteries of Patients With Giant Cell Arteritis

2011

Objective Giant cell (temporal) arteritis (GCA) is a vasculitis that mainly affects the large and medium arteries, especially the branches of the proximal aorta. Interleukin-32 (IL-32) is a recently described Th1 proinflammatory cytokine, and is mainly induced by interferon-γ (IFNγ), IL-1β, and tumor necrosis factor α (TNFα). This study was undertaken to investigate the expression and tissue distribution of IL-32 in artery biopsy specimens from patients with GCA. Methods Quantitative gene expression analysis of IL-32, IL-1β, TNFα, IFNγ, IL-6, and IL-27 was performed in artery biopsy specimens obtained from 18 patients with GCA and 15 controls. Immunohistochemistry analysis was performed to …

MalePathologyInterleukin-1betaMessenger80 and overImmunology and AllergyPharmacology (medical)Giant Cell ArteritiAged 80 and overeducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionInterleukin-17StatisticsArteriesMiddle AgedFlow CytometryImmunohistochemistryTh1 responseFemaleInterleukin 17VasculitisInterleukin-32; Giant Cell Arteritis; Th1 responsemedicine.medical_specialtyGiant Cell ArteritisImmunologyPopulationBiologyStatistics NonparametricProinflammatory cytokineInterferon-gammaRheumatologymedicine.arterymedicineHumansNonparametricRNA MessengerArteritiseducationAgedAortaAged; Aged 80 and over; Arteries; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; Interferon-gamma; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukins; Male; Middle Aged; RNA Messenger; Reverse Transcriptase Polymerase Chain Reaction; Statistics Nonparametric; Th1 Cells; Tumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alphaInterleukinsTh1 Cellsmedicine.diseaseInterleukin-32Giant cell arteritisGiant cellImmunologyRNA
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Interleukin-36α axis is modulated in patients with primary Sjögren's syndrome.

2015

Summary The aim of this study was to investigate the expression of the interleukin (IL)-36 axis in patients with primary Sjögren's syndrome (pSS). Blood and minor labial salivary glands (MSG) biopsies were obtained from 35 pSS and 20 non-Sjögren's syndrome patients (nSS) patients. Serum IL-36α was assayed by enzyme-linked immunosorbent assay (ELISA). IL-36α, IL-36R, IL-36RA, IL-38, IL-22, IL-17, IL-23p19 and expression in MSGs was assessed by reverse transcription–polymerase chain reaction (RT–PCR), and tissue IL-36α and IL-38 expression was also investigated by immunohistochemistry (IHC). αβ and γδ T cells and CD68+ cells isolated from MSGs were also studied by flow cytometry and confocal …

MaleReceptors Antigen T-Cell alpha-betaT-LymphocytesSalivary GlandsIL-36aIL-36a IL-38 IL36RA Sjogren's syndrome γδT cellsImmunology and AllergyMedicinemedicine.diagnostic_testSalivary glandbiologyCD68γδT cellsInterleukin-17TranslationalIL-36a; IL-38; IL36RA; Sjögren's syndrome; γδ T cellsInterleukinReceptors Antigen T-Cell gamma-deltaMiddle Agedmedicine.anatomical_structureSjogren's SyndromeImmunohistochemistryFemaleSjögren's syndromeInterleukin 17Signal TransductionAdultmedicine.medical_specialtyCD3ImmunologyPrimary Cell CultureAntigens Differentiation Myelomonocyticγδ T cellsIL36RAFlow cytometrystomatognathic systemAntigens CDInternal medicineHumansbusiness.industryInterleukinsReceptors InterleukinIL-38stomatognathic diseasesSettore MED/16 - ReumatologiaEndocrinologyGene Expression RegulationCell cultureCase-Control StudiesImmunologybiology.proteinInterleukin-23 Subunit p19businessInterleukin-1
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T helper type 17-related cytokine expression is increased in the bronchial mucosa of stable chronic obstructive pulmonary disease patients.

2009

Summary There are increased numbers of activated T lymphocytes in the bronchial mucosa of stable chronic obstructive pulmonary disease (COPD) patients. T helper type 17 (Th17) cells release interleukin (IL)-17 as their effector cytokine under the control of IL-22 and IL-23. Furthermore, Th17 numbers are increased in some chronic inflammatory conditions. To investigate the expression of interleukin (IL)-17A, IL-17F, IL-21, IL-22 and IL-23 and of retinoic orphan receptor RORC2, a marker of Th17 cells, in bronchial biopsies from patients with stable COPD of different severity compared with age-matched control subjects. The expression of IL-17A, IL-17F, IL-21, IL-22, IL-23 and RORC2 was measure…

MaleTranslational StudiesReceptors Retinoic Acidmedicine.medical_treatmentImmunologyautoimmunity bronchial biopsies emphysema neutrophilsInflammationBronchiInterleukin-23Polymerase Chain ReactionStatistics NonparametricPulmonary Disease Chronic ObstructiveAutoimmunity bronchial biopsies emphysema neutrophils pathologymedicineInterleukin 23Immunology and AllergyHumansRNA MessengerAgedDNA PrimersCOPDAnalysis of VarianceMucous MembraneReceptors Thyroid Hormonebusiness.industryInterleukinsRespiratory diseaseInterleukin-17SmokingInterleukinT-Lymphocytes Helper-InducerMiddle AgedNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseImmunohistochemistryrespiratory tract diseasesRespiratory Function TestsCytokineCase-Control StudiesImmunologyFemaleInterleukin 17medicine.symptombusinessCD8
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ID: 186

2015

In the past years, and clear pathogenic role was shown for Th17 cells in the development of autoimmune diseases. In particular, these cells were shown to play a critical roIn the past years, and clear pathogenic role was shown for Th17 cells in the development of autoimmune diseases. In particular, these cells were shown to play a critical role in the development of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. One of the major cytokines Th17 cells produce is IL-17A, a cytokine of the IL-17 family. IL-17A, as well as it homologue IL-17F bind and trigger cells via the IL-17 receptor A/C complex. We have used a series of mice with deficiencies in the…

Multiple sclerosismedicine.medical_treatmentImmunologyExperimental autoimmune encephalomyelitisHematologyBiologymedicine.diseasemedicine.disease_causeBiochemistryAutoimmunityCytokineImmunologymedicineImmunology and AllergyInterleukin 17ReceptorMolecular BiologyTranscription factorFunction (biology)Cytokine
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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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IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice.

2009

Abstract Resistance to leishmaniasis in C57BL/6 mice depends on Th1/Tc1 cells. BALB/c mice preferentially develop Th2 immunity and succumb to infection. We now assessed the role of IL-17 in cutaneous leishmaniasis. During the course of Leishmania major infection, BALB/c CD4 cells and neutrophils produced increased amounts of IL-17 as compared with cells from C57BL/6 mice. This increase was associated with significantly increased IL-23 release from L. major-infected BALB/c dendritic cells (DC), whereas IL-6 and TGF-β1 production by BALB/c and C57BL/6 DC were comparable. Interestingly, lesion sizes in infected IL-17-deficient BALB/c mice were dramatically smaller and failed to progress as com…

NeutrophilsImmunologyLeishmaniasis CutaneousBiologyInterleukin-23ArticleLesionMiceImmune systemTh2 CellsCutaneous leishmaniasisSpecies SpecificityImmunitymedicineImmunology and AllergyAnimalsLeishmania majorGenetic Predisposition to DiseaseInterleukin 4Cells CulturedLeishmania majorMice KnockoutImmunity CellularMice Inbred BALB CInterleukin-17Cell DifferentiationDendritic Cellsmedicine.diseasebiology.organism_classificationUp-RegulationMice Inbred C57BLInterleukin 10ImmunologyDisease ProgressionInterleukin 17medicine.symptomJournal of immunology (Baltimore, Md. : 1950)
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OP0017 Gut-Derived IL-23R+CD3+CD4-CD8-CD56+T-BET+NKP44+ Cells Are Expanded in the Peripheral Blood, Synovial Fluid and Bone Marrow of Patients with A…

2014

Background Chronic gut inflammation occurring in AS patients has been linked to active axial inflammation and the gut has been proposed as the main site of IL-23 production in AS patients. IL-23 has been demonstrated to be essential in murine enthesitis by acting on a unique subset of entheseal resident T cells that share some immunological features with a subset of IL-23-responsive gut derived innate lymphoid cells (type III ILCs). Objectives Aim of the study was to better characterize the immunologic origin and the behavior of ILCs in the gut, synovial fluid and bone marrow of AS patients. Methods Consecutive ileal gut biopsies were obtained from 20 HLA-B27 + AS patients with axial active…

Pathologymedicine.medical_specialtybusiness.industryImmunologyInnate lymphoid cellPeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular BiologyInterleukin 22medicine.anatomical_structureLymphatic systemRheumatologyGammopathymedicineImmunology and AllergySynovial fluidBone marrowInterleukin 17businessAnnals of the Rheumatic Diseases
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Shikonin reduces the tumour formation and IL-17 in a model of colorectal cancer associated to chronic colitis in C57BL/6 mice

2016

PharmacologyGerontologyC57BL/6biologybusiness.industryColorectal cancerOrganic ChemistryPharmaceutical Sciencemedicine.diseasebiology.organism_classificationTumor formationAnalytical ChemistryComplementary and alternative medicineDrug DiscoveryCancer researchMolecular MedicineMedicineInterleukin 17businessChronic colitisPlanta Medica
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Critical Regulation of Early Th17 Cell Differentiation by Interleukin-1 Signaling

2009

SummaryT helper (Th) 17 cells have been recently discovered in both mouse and human. Here we show that interleukin-1 (IL-1) signaling on T cells is critically required for the early programming of Th17 cell lineage and Th17 cell-mediated autoimmunity. IL-1 receptor1 expression in T cells, which was induced by IL-6, was necessary for the induction of experimental autoimmune encephalomyelitis and for early Th17 cell differentiation in vivo. Moreover, IL-1 signaling in T cells was required in dendritic cell-mediated Th17 cell differentiation from naive or regulatory precursors and IL-1 synergized with IL-6 and IL-23 to regulate Th17 cell differentiation and maintain cytokine expression in effe…

Regulation of gene expressionEffectorCellular differentiationExperimental autoimmune encephalomyelitisImmunologychemical and pharmacologic phenomenahemic and immune systemsBiologymedicine.diseaseMolecular biologyCell biologyInfectious DiseasesCELLIMMUNOCell polaritymedicineImmunology and AllergyInterleukin 17Signal transductionMOLIMMUNOTranscription factorImmunity
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