Search results for " Interleukin-17"

showing 10 items of 11 documents

Subclinical gut inflammation in ankylosing spondylitis

2015

Purpose of review Subclinical gut inflammation has been described in a significant proportion of patients with ankylosing spondylitis (AS), up to 10% of them developing it during the time of clinically overt inflammatory bowel disease. Histologic, immunologic, and intestinal microbiota alterations characterize the AS gut. Recent findings Microbial dysbiosis as well as alterations of innate immune responses have been demonstrated in the gut of AS. Furthermore, a growing body of evidence suggests that the gut of AS patients may be actively involved in the pathogenesis of AS through the production of proinflammatory cytokines, such as IL-23p19, and the differentiation of potentially pathogenic…

0301 basic medicineAnkylosing spondylitis; Gut inflammation; Innate lymphoid cells; Interleukin-17; Interleukin-23; Adaptive Immunity; Animals; Cytokines; Disease Models Animal; Dysbiosis; Gastrointestinal Microbiome; Humans; Immunity Innate; Inflammation; Inflammatory Bowel Diseases; Intestines; Macrophages; Mice; Spondylitis Ankylosing; Rheumatology; Medicine (all)MacrophageAdaptive ImmunityInterleukin-23Inflammatory bowel diseaseGastroenterologyMiceInterleukin 23InnateMedicineSubclinical infectionMedicine (all)Interleukin-17digestive oral and skin physiologyInnate lymphoid cellIntestineIntestinesCytokinesmedicine.symptomHumanAnkylosingmedicine.medical_specialtyDisease ModelInflammationdigestive system03 medical and health sciencesRheumatologyInternal medicineInnate lymphoid cellAnimalsHumansSpondylitis AnkylosingCytokineSpondylitisGut inflammationSpondylitiInflammationAnkylosing spondylitisAnimalbusiness.industryMacrophagesInflammatory Bowel DiseaseImmunityInflammatory Bowel Diseasesmedicine.diseaseImmunity InnateDysbiosiGastrointestinal MicrobiomeAnkylosing spondylitiDisease Models Animal030104 developmental biologyDysbiosisbusinessDysbiosisCurrent Opinion in Rheumatology
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Characteristic of chronic plaque psoriasis patients treated with biologics in Italy during the COVID-19 pandemic. risk analysis from the PSO-BIO-COVI…

2021

Background The susceptibility of patients with chronic plaque psoriasis and the risks or benefits related to the use of biological therapies for COVID-19 are unknown. Few data about prevalence, clinical course and outcomes of COVID-19 among psoriatic patients were reported. The aims of this study were 1) to assess the prevalence and severity of COVID-19 in psoriatic patients treated with biologic agents during the first phase of the emergency (22 February to 22 April 2020) in Italy, and 2) to report the clinical outcomes of patients who have been exposed to individuals with confirmed SARS-CoV-2 infection. Methods Patients with moderate-to-severe chronic plaque psoriasis, aged ≥18 years and …

0301 basic medicineMaleClinical BiochemistryDiseaseCohort Studies0302 clinical medicineDrug DiscoveryReceptors80 and overMedicineAged 80 and overeducation.field_of_studyIncidence (epidemiology)IncidenceInterleukin-17psoriasisMiddle Ageddermatologysars-CoV-2Italybiological therapy030220 oncology & carcinogenesisCohortBiological ProductCOVID-19; biological therapy; dermatology; psoriasis; sars-CoV-2FemaleSettore MED/35 - MALATTIE CUTANEE E VENEREEbiological therapy; COVID-19; dermatology; psoriasis; sars-CoV-2; Adult; Aged; Aged 80 and over; Biological Products; Biological Therapy; COVID-19; Chronic Disease; Cohort Studies; Female; Humans; Incidence; Interleukin-17; Italy; Male; Middle Aged; Pandemics; Psoriasis; Receptors Interleukin; Risk Assessment; Tumor Necrosis Factor-alpha; Young AdultCohort studyHumanAdultmedicine.medical_specialtyPopulationRisk AssessmentCOVID-19; psoriasis; biological therapy; dermatology; sars-CoV-203 medical and health sciencesYoung AdultSettore MED/35Internal medicinePsoriasisPsoriasis.HumanseducationPandemicsAgedPharmacologyPsoriasiBiological ProductsPandemicbiological therapy; COVID-19; dermatology; psoriasis; sars-CoV-2business.industryTumor Necrosis Factor-alphaCOVID-19Receptors InterleukinBiological productInterleukinmedicine.diseaseClinical trial030104 developmental biologyChronic DiseaseCOVID-19; SARS-CoV-2; biological therapy; dermatology; psoriasisCohort Studiebusiness
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Interleukin-25 Axis Is Involved in the Pathogenesis of Human Primary and Experimental Murine Sjögren's Syndrome

2018

Objective To investigate the role of the interleukin-25 (IL-25)/IL-17 receptor B (IL-17RB) axis in experimental Sjogren's syndrome (SS) and in patients with primary SS and primary SS-associated lymphoma. Methods Expression of IL-25, IL-17RB, IL-17B, and tumor necrosis factor receptor-associated factor 6 (TRAF6) was analyzed on minor salivary gland (SG) samples from patients with primary SS and on parotid gland samples from patients with primary SS-associated B cell non-Hodgkin's lymphoma (NHL). IL-17RB expression and the frequencies of natural group 2 innate lymphoid cells (ILC2s), inflammatory ILC2s, and M2-polarized macrophages were assessed by flow cytometry in SG mononuclear cells and p…

0301 basic medicineMaleLymphomaMacrophageImmunologyPeripheral blood mononuclear cellSalivary GlandSalivary GlandsFlow cytometry03 medical and health sciencesMice0302 clinical medicineRheumatologyInterleukin 25AnimalsHumansMedicineImmunology and AllergyLymphocytesB cellAgedReceptors Interleukin-17medicine.diagnostic_testbusiness.industryAnimalMacrophagesInnate lymphoid cellInterleukin-17Middle Agedmedicine.diseaseImmunity InnateLymphomaSettore MED/16 - Reumatologia030104 developmental biologymedicine.anatomical_structureSjogren's SyndromeImmunologyImmunology and Allergy; Rheumatology; ImmunologyLeukocytes MononuclearRituximabTumor necrosis factor alphaFemaleLymphocytebusiness030215 immunologymedicine.drugHuman
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Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibitio…

2018

Visual Abstract

0301 basic medicinemedicine.medical_specialtylcsh:Diseases of the circulatory (Cardiovascular) systemIl17ra interleukin-17 receptor A (gene name)medicine.medical_treatmentInterleukin-17 receptormacrophage030204 cardiovascular system & hematologyLesionPRECLINICAL RESEARCH03 medical and health sciencesPCR polymerase chain reaction0302 clinical medicineInternal medicinemedicineMacrophageReceptorbusiness.industryCKD chronic kidney diseaseLDLr low-density lipoprotein receptorIL interleukinBlockadeEndothelial stem cell030104 developmental biologyEndocrinologyCytokinelcsh:RC666-701Interleukin 17medicine.symptomatherosclerosisCardiology and Cardiovascular Medicinebusinessinterleukin 17chronic kidney diseaseJACC: Basic to Translational Science
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The transcription factor NFATc2 controls IL-6–dependent T cell activation in experimental colitis

2008

The nuclear factor of activated T cells (NFAT) family of transcription factors controls calcium signaling in T lymphocytes. In this study, we have identified a crucial regulatory role of the transcription factor NFATc2 in T cell–dependent experimental colitis. Similar to ulcerative colitis in humans, the expression of NFATc2 was up-regulated in oxazolone-induced chronic intestinal inflammation. Furthermore, NFATc2 deficiency suppressed colitis induced by oxazolone administration. This finding was associated with enhanced T cell apoptosis in the lamina propria and strikingly reduced production of IL-6, -13, and -17 by mucosal T lymphocytes. Further studies using knockout mice showed that IL-…

Adjuvants Immunologic; Animals; Humans; Interleukin-13; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mice; Mice Inbred BALB C; Mice Knockout; Mice SCID; Models Biological; NFATC Transcription Factors; Oxazolone; T-LymphocytesT cellT-LymphocytesImmunologyMice SCIDBiologyLymphocyte ActivationInflammatory bowel diseaseModels BiologicalArticleOxazoloneTCIRG1chemistry.chemical_compoundMiceAdjuvants ImmunologicmedicineImmunology and AllergyCytotoxic T cellAnimalsHumansColitisMice KnockoutMice Inbred BALB CInterleukin-13NFATC Transcription FactorsInterleukin-6Interleukin-17OxazoloneArticlesmedicine.diseasemedicine.anatomical_structurechemistryImmunologyInterleukin 13Cancer researchInterleukin 17The Journal of Experimental Medicine
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Mast Cells and Th17 Cells Contribute to the Lymphoma-Associated Pro-Inflammatory Microenvironment of Angioimmunoblastic T-Cell Lymphoma

2010

Reports focusing on the immunological microenvironment of peripheral T-cell lymphomas (PTCL) are rare. Here we studied the reciprocal contribution of regulatory (Treg) and interleukin-17-producing (Th17) T-cells to the composition of the lymphoma-associated microenvironment of angioimmunoblastic T-cell lymphoma (AITL) and PTCL not otherwise specified on tissue microarrays from 30 PTCLs not otherwise specified and 37 AITLs. We found that Th17 but not Treg cells were differently represented in the two lymphomas and correlated with the amount of mast cells (MCs) and granulocytes, which preferentially occurred in the cellular milieu of AITL cases. We observed that MCs directly synthesized inter…

Angioimmunoblastic T-cell lymphomaLymphomaInflammationBiologymedicine.disease_causeCXCR3Lymphoma T-CellCXCR5Pathology and Forensic MedicineAutoimmunityAnimals Chemokine CXCL13; immunology Cytokines; genetics/immu/nology Forkhead Transcription Factors; immunology Gene Expression Profiling Humans Immunoblastic Lymphadenopathy; immunology/pathology Inflammation; immunology Interleukin-17; immunology Interleukin-6; immunology Lymphoma; T-Cell; immunology/pathology Mast Cells; immunology Microarray Analysis Th17 Cells; immunology Tumor MicroenvironmentimmunologymedicineTumor MicroenvironmentAnimalsHumansMast CellsInflammationTumor microenvironmentInterleukin-6Gene Expression ProfilingInterleukin-17Forkhead Transcription FactorsMast cellmedicine.diseaseT-CellMicroarray AnalysisChemokine CXCL13humanitiesgenetics/immu/nologyLymphomamedicine.anatomical_structureImmunoblastic LymphadenopathyImmunologyCytokinesimmunology/pathologyTh17 CellsMast Cell microenvironment angioimmunoblasticmedicine.symptomRegular Articles
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An Alternative Pathway of Imiquimod-Induced Psoriasis-Like Skin Inflammation in the Absence of Interleukin-17 Receptor A Signaling

2013

Topical application of imiquimod (IMQ) on the skin of mice induces inflammation with common features found in psoriatic skin. Recently, it was postulated that IL-17 has an important role both in psoriasis and in the IMQ model. To further investigate the impact of IL-17RA signaling in psoriasis, we generated IL-17 receptor A (IL-17RA)-deficient mice (IL-17RA(del)) and challenged these mice with IMQ. Interestingly, the disease was only partially reduced and delayed but not abolished when compared with controls. In the absence of IL-17RA, we found persisting signs of inflammation such as neutrophil and macrophage infiltration within the skin. Surprisingly, already in the naive state, the skin …

ChemokineInflammationImiquimodDermatologyInterleukin-17 receptorBiochemistryMiceAdjuvants ImmunologicPsoriasismedicineAnimalsPsoriasisMacrophageMolecular BiologySkinMice KnockoutImiquimodReceptors Interleukin-17biologyInterleukin-6InterleukinsMacrophagesInterleukin-17Cell Biologymedicine.diseaseDisease Models AnimalCXCL2Neutrophil InfiltrationImmunologyAminoquinolinesbiology.proteinFemaleTumor necrosis factor alphamedicine.symptomSignal Transductionmedicine.drugJournal of Investigative Dermatology
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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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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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Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

2009

Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cel…

Regulatory T cellmedicine.medical_treatmentCellular differentiationImmunologyPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicMast cell; T regulatory cell; Immune responseBiologyLymphocyte ActivationT-Lymphocytes RegulatoryBiochemistryImmune toleranceMiceMice CongenicmedicineImmune ToleranceMast CellT regulatory cellImmune responseCells CulturedCell ProliferationAnimalInterleukin-6Experimental autoimmune encephalomyelitisInterleukin-17hemic and immune systemsCell DifferentiationT lymphocyteT-Lymphocytes Helper-InducerHematologyCell BiologyReceptors OX40medicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structureCytokineImmunologyAnimals; Cell Differentiation; Cell Proliferation; Cells Cultured; Immune Tolerance; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mast Cells; Membrane Glycoproteins; Mice; Mice Congenic; Mice Inbred C57BL; Mice Transgenic; Receptors OX40; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Hematology; Biochemistry; Cell Biology; ImmunologyInterleukin 17Membrane GlycoproteinTumor Necrosis FactorSignal Transduction
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