Search results for "Interleukin-23"

showing 10 items of 47 documents

Insufficient generation of Th17 cells in IL-23p19-deficient BALB/c mice protects against progressive cutaneous leishmaniasis

2017

Healing of leishmaniasis-a parasitic skin disease-is associated with high levels of secreted interferon (IFN)γ and IL-12 in resistant C57BL/6 mice and humans. Susceptible BALB/c mice predominantly react with a Th17/Th2/Treg-related immune response and finally succumb to infection. Previously, we showed that BALB/c IL-17A-/- mice are protected against Leishmania (L.) major infections, indicating that IL-17A-predominantly produced by Th17 cells-plays an important role for disease outcome. We now investigated DC-derived cytokines and finally identified IL-23p19 as key cytokine responsible for induction of Leishmania-specific Th17 cells that play an important role for progressive disease in sus…

0301 basic medicinemedicine.medical_treatmentLeishmaniasis CutaneousDermatologyPolymerase Chain ReactionBiochemistryBALB/cInterferon-gammaMice03 medical and health sciences0302 clinical medicineImmune systemCutaneous leishmaniasisInterferonInterleukin 23AnimalsMedicineMolecular BiologyLeishmania majorMice Inbred BALB Cbiologybusiness.industryLeishmaniasisDendritic CellsLeishmaniabiology.organism_classificationmedicine.disease030104 developmental biologyCytokineImmunologyDisease ProgressionInterleukin-23 Subunit p19CytokinesTh17 Cellsbusiness030215 immunologymedicine.drugExperimental Dermatology
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Contribution of IL-17-producing {gamma}{delta} T cells to the efficacy of anticancer chemotherapy.

2011

IL-17 production by γδ T cells is required for tumor cell infiltration by IFN-γ–producing CD8+ T cells and inhibition of tumor growth in response to anthracyclines.

Adoptive cell transferMESH : AgedMESH : Equipment DesignCD8-Positive T-LymphocytesMESH: CatheterizationInterleukin-23MESH: Long-Term CareMice0302 clinical medicineMESH : CatheterizationT-Lymphocyte SubsetsMESH: NursingImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyInterferon gammaMESH: Quality of Health CareMESH: Professional Review OrganizationsMESH: AgedMESH : Gels0303 health sciencesMice Inbred BALB CCell DeathInterleukin-17MESH : Methylene BlueMESH : Quality of Health CareReceptors Antigen T-Cell gamma-deltaChemotherapy regimenMESH: Transplantation Autologous3. Good healthMESH: Cosmetic TechniquesTreatment Outcomemedicine.anatomical_structureMESH : Cadaver[SDV.IMM]Life Sciences [q-bio]/ImmunologyImmunogenic cell deathSarcoma ExperimentalInterleukin 17MESH : DissectionMESH : Long-Term CareMESH: Nursing CareMESH: Adipose Tissuemedicine.drugSignal TransductionMESH : Transplantation Autologous[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Feasibility StudiesMESH: GelsT cellMESH : MaleImmunologyMESH: DissectionAntineoplastic AgentsBiologyMESH : NursingMESH : Adipose TissueArticleMESH : Facial Muscles03 medical and health sciencesInterferon-gammaLymphocytes Tumor-InfiltratingImmune systemAntigenCell Line TumorMESH: Patient Care PlanningmedicineMESH: CadaverAnimalsMESH : Patient Care Planning030304 developmental biologyMESH: Humansbusiness.industryMESH: Facial MusclesT-cell receptorMESH : HumansCorrectionMESH: MaleMice Inbred C57BLMESH : Cosmetic TechniquesDoxorubicinImmunologyCancer researchMESH : Nursing CareMESH : Professional Review OrganizationsbusinessMESH: Feasibility StudiesCD8030215 immunologyMESH: Methylene BlueMESH: Equipment Design
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Potential involvement of IL-22 and IL-22-producing cells in the inflamed salivary glands of patients with Sjogren's syndrome.

2012

OBJECTIVES: In chronic inflammatory disorders, interleukin (IL)-22 may act either as a protective or as a pro-inflammatory cytokine. At mucosal sites, IL-22 is mainly produced by CD4(+) T cells and by a subset of mucosal natural killer (NK) cells expressing the receptor NKp44 (NKp44(+) NK cells). The aim of this study was to investigate the IL-22 expression in the salivary glands of patients with primary Sjögren's syndrome (pSS). METHODS: Minor salivary gland biopsies were obtained from 19 patients with pSS and 16 with non-specific chronic sialoadenitis. Quantitative gene expression analysis by TaqMan real-time PCR and immunohistochemistry for IL-17, IL-22, IL-23 and STAT3 (signal transduce…

AdultCD4-Positive T-LymphocytesMaleSTAT3 Transcription FactorAnkylosing Spondylitis IL-22 NKp44NK cells intestinal inflammationmedicine.medical_treatmentImmunologySalivary Glands MinorInterleukin-23General Biochemistry Genetics and Molecular BiologySialadenitisInterleukin 22PathogenesisRheumatologyintestinal inflammationIL-22Immunology and AllergyMedicineHumansRNA MessengerSTAT3ReceptorAgedAnkylosing SpondylitibiologySalivary glandNatural Cytotoxicity Triggering Receptor 2business.industryReverse Transcriptase Polymerase Chain ReactionInterleukinsInterleukin-17InterleukinMiddle AgedNKp44NK cellKiller Cells NaturalSettore MED/16 - ReumatologiaCytokinemedicine.anatomical_structureSjogren's SyndromeCase-Control StudiesImmunologybiology.proteinImmunohistochemistryFemalebusinessAnnals of the rheumatic diseases
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Proinflammatory CX3CR1+CD59+Tumor Necrosis Factor–Like Molecule 1A+Interleukin‐23+ Monocytes Are Expanded in Patients With Ankylosing Spondylitis and…

2018

Objective: Gut-derived innate lymphoid cell 3 (ILC3) has been shown to participate in the pathogenesis of ankylosing spondylitis (AS). CX3CR1+ mononuclear phagocytes (MNPs) have been demonstrated to modulate ILC3 function in the gut. This study was undertaken to investigate the role of proinflammatory CX3CR1+CD59+ MNPs in modulating ILC3 function in AS patients. Methods: MNP subsets in the blood of AS patients and controls were analyzed by flow cytometry. The presence of CX3CR1+CD59+ cells in tissue was confirmed by confocal microscopy. Expression of the proinflammatory chemokines CX3CL1 and CCL2 and decoy receptor 6 (DcR-6) was analyzed. Peripheral CX3CR1+CD59+ cells were cocultured with I…

AdultMale0301 basic medicineChemokineImmunologyPopulationCX3C Chemokine Receptor 1CD11cCD59 Antigenschemical and pharmacologic phenomenaCCL2Interleukin-23MonocytesProinflammatory cytokineFlow cytometry03 medical and health sciences0302 clinical medicineRheumatologymedicineHumansImmunology and AllergySpondylitis AnkylosingLymphocytesCX3CL1educationMononuclear Phagocyte System030203 arthritis & rheumatologyeducation.field_of_studybiologymedicine.diagnostic_testChemistryInnate lymphoid cellMiddle AgedImmunity Innate030104 developmental biologyReceptors Tumor Necrosis Factor Type ICase-Control Studiesbiology.proteinCancer researchFemaleArthritis & Rheumatology
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Both IL-12p70 and IL-23 are synthesized during active Crohnʼs disease and are down-regulated by treatment with anti-IL-12 p40 monoclonal antibody

2005

Background: Interleukin (IL)-12p70 and IL-23 are key T helper-1 (TH1) cytokines that drive the inflammation seen in numerous models of intestinal inflammation. These molecules contain an identical p40 chain that is bound to a p35 chain in IL-12 and a p19 chain in IL-23, making both potentially susceptible to modulation by an anti-IL-12p40 monoclonal antibody (mAb). Methods: In the present study, we sought to determine whether active inflammation in Crohn's disease (CD) is associated with the increased synthesis of both of these cytokines and whether patients treated with an anti-IL-12p40 mAb down-regulate IL-23 as well as IL-12p70 as previous reported. Results: To this end we initially dete…

AdultMaleAdolescentBiopsyT-Lymphocytesmedicine.medical_treatmentT cellDown-RegulationInterleukin-23Crohn DiseaseInterleukin 23medicineHumansImmunology and AllergyCells CulturedAgedLamina propriaMucous MembraneCD40biologyInterleukin-12 Subunit p40Interleukin-6InterleukinsMacrophagesGastroenterologyAntibodies MonoclonalInterleukinMiddle AgedInterleukin-12Protein Subunitsmedicine.anatomical_structureCytokineImmunologyInterleukin-23 Subunit p19biology.proteinInterleukin 12FemaleTumor necrosis factor alphaInterleukin-1Inflammatory Bowel Diseases
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Replication of interleukin 23 receptor and autophagy-related 16-like 1 association in adult- and pediatric-onset inflammatory bowel disease in Italy.

2008

AIM: To investigate gene variants in a large Italian inflammatory bowel disease (IBD) cohort, and to analyze the correlation of sub-phenotypes (including age at diagnosis) and epistatic interaction with other IBD genes. METHODS: Total of 763 patients with Crohn's disease (CD, 189 diagnosed at age < 19 years), 843 with ulcerative colitis (UC, 179 diagnosed < 19 years), 749 healthy controls, and 546 healthy parents (273 trios) were included in the study. The rs2241880 [autophagy-related 16-like 1 (ATG16L1)], rs11209026 and rs7517847 [interleukin 23 receptor (IL23R)], rs2066844, rs2066845, rs2066847 (CARD15), rs1050152 (OCTN1), and rs2631367 (OCTN2) gene variants were genotyped. RESULTS: The f…

AdultMaleInterleukin-23 receptorAdolescentGenotypeOrganic Cation Transport ProteinsIBDNod2 Signaling Adaptor ProteinAutophagy-Related Proteinsdigestive systemPolymorphism Single NucleotideInflammatory bowel diseaseYoung AdultSettore MED/38 - Pediatria Generale E SpecialisticaCrohn DiseaseIL23RClinical ResearchmedicineGenetic predispositionHumansGenetic Predisposition to DiseaseAge of OnsetYoung adultChildSolute Carrier Family 22 Member 5ReceptorAgedCrohn's diseaseSymportersbusiness.industryGastroenterologyInfantReceptors InterleukinGeneral MedicineMiddle AgedInflammatory Bowel Diseasesmedicine.diseaseUlcerative colitisdigestive system diseasesLogistic ModelsItalyCase-Control StudiesChild PreschoolImmunologyFemaleAge of onsetCarrier Proteinsbusiness
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Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

2009

Objective Subclinical gut inflammation is common in spondylarthritis, but the immunologic abnormalities underlying this process are undefined. Perturbation of the interleukin-23 (IL-23)/Th17 axis has emerged as a fundamental trigger of chronic inflammation. This study was undertaken to investigate the expression and tissue distribution of IL-23/Th17–related molecules in Crohn's disease (CD) and in subclinical gut inflammation in ankylosing spondylitis (AS). Methods Quantitative gene expression analysis of Th1/Th2 and IL-23/Th17 responses was performed in intestinal biopsy samples obtained from 12 patients with CD, 15 patients with AS, and 13 controls. IL-23 tissue distribution and identific…

AdultMalePaneth Cellschronic inflammationPathologymedicine.medical_specialtyImmunologyGene ExpressionInflammationMonocytesTh2 CellsRheumatologyIntestinal mucosaIleumankylosing spondylitisPrevalencemedicineInterleukin 23HumansImmunology and Allergyinterleukin-23 (IL-23); Th 17;chronic inflammation; Crohn's disease; ankylosing spondylitisSpondylitis AnkylosingPharmacology (medical)IleitisRNA MessengerIntestinal MucosaSpondylitisinterleukin-23 (IL-23)Subclinical infectionAnkylosing spondylitisbusiness.industryInterleukin-17IleitisMiddle AgedTh1 Cellsmedicine.diseaseUp-RegulationCrohn's diseaseSTAT1 Transcription FactorTh 17ImmunologyInterleukin-23 Subunit p19FemaleInterleukin 17medicine.symptombusinessArthritis &amp; Rheumatism
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IL-34 is overexpressed in the inflamed salivary glands of patients with Sjogren's syndrome and is associated with the local expansion of pro-inflamma…

2013

Objectives To investigate the expression of IL-34 in labial salivary glands (LSGs) of patients with primary SS (p-SS) and its role in inducing a pro-inflammatory monocyte phenotype. Methods LSG biopsies were obtained from 20 patients with p-SS and 10 patients with non-Sjogren's sicca syndrome (n-SS). The expression of IL-34, IL-1β, TNF-α, IL-17 and IL-23 was assessed by real-time PCR. IL-34 expression was also investigated in LSGs by immunohistochemistry. The frequencies of subpopulations of CD14(+) monocytes were evaluated by flow cytometry among isolated mononuclear cells from peripheral blood and salivary glands from both patients and controls. The role of recombinant IL-34 on isolated p…

AdultMalePathologymedicine.medical_specialtyCD14Interleukin-1betaLipopolysaccharide ReceptorsInflammationCD16Interleukin-23Peripheral blood mononuclear cellMonocytesSalivary GlandsRheumatologySicca syndromemedicineHumansPharmacology (medical)interleukin-34 Sjögren’s syndrome monocytesAgedInflammationSalivary glandTumor Necrosis Factor-alphabusiness.industryInterleukinsMonocyteInterleukin-17Receptors IgGMiddle AgedFlow CytometrySettore MED/16 - ReumatologiaSjogren's Syndromemedicine.anatomical_structureImmunologyInterleukin 34Femalemedicine.symptombusinessRheumatology
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Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of patients with ankylosing spondylitis …

2013

OBJECTIVES: Interleukin (IL)-23 has been implicated in the pathogenesis of ankylosing spondylitis (AS). The aim of the study was to clarify the mechanisms underlying the increased IL-23 expression in the gut of AS patients. METHODS: Consecutive gut biopsies from 30 HLA-B27(+) AS patients, 15 Crohn's disease (CD) patients and 10 normal subjects were obtained. Evidence for HLA-B27 misfolding was studied. Unfolded protein response (UPR) and autophagy were assessed by RT-PCR and immunohistochemistry. The contribution of UPR and autophagy in the regulation of IL-23 expression was evaluated in in vitro experiments on isolated lamina propria mononuclear cells (LPMCs). RESULTS: Intracellular coloca…

AdultMaleProtein FoldingBiopsyImmunologyATG5Gene ExpressionInflammationdigestive systemArticleGeneral Biochemistry Genetics and Molecular BiologyATG12Young AdultCrohn DiseaseRheumatologyDownregulation and upregulationSettore BIO/13 - Biologia Applicataankylosing spondylitisAutophagymedicineInterleukin 23HumansImmunology and AllergySpondylitis AnkylosingHLA-B27 AntigenAgedMucous Membranebusiness.industryAutophagyInterleukinIleitisMiddle AgedIntestinesInterleukin 23Settore MED/16 - ReumatologiaImmunologyInterleukin-23 Subunit p19Unfolded Protein ResponseUnfolded protein responseFemalemedicine.symptombusinessAnnals of the Rheumatic Diseases
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Interleukin-22 and interleukin-22-producing NKp44+ natural killer cells in subclinical gut inflammation in ankylosing spondylitis

2012

Objective The intestinal inflammation observed in patients with ankylosing spondylitis (AS) is characterized by an overexpression of interleukin-23 (IL-23). IL-23 is known to regulate IL-22 production through lamina propria NKp44+ natural killer (NK) cells, which are thought to be involved in protective mucosal mechanisms. This study was undertaken to evaluate the frequency of NKp44+ NK cells and the expression of IL-22 in the ileum of AS patients. Methods Tissue NKp44+ NK cells, NKp46+ NK cells, and IL-22–producing cells were analyzed by flow cytometry. Quantitative gene expression analysis of IL-22, IL-23, IL-17, STAT-3, and mucin 1 (MUC-1) was performed by reverse transcriptase–polymeras…

AdultMaleSTAT3 Transcription FactorImmunologyIleumBiologyInterleukin-23Peripheral blood mononuclear cellFlow cytometryAnkylosing spondylitis IL-22 intestinal inflammation intestinal inflammationInterleukin 22Interleukin 21RheumatologyIleumintestinal inflammationIL-22medicineHumansImmunology and AllergySpondylitis AnkylosingPharmacology (medical)Intestinal MucosaInflammationLamina propriaNatural Cytotoxicity Triggering Receptor 2medicine.diagnostic_testInterleukinsMucin-1MucinMiddle AgedKiller Cells NaturalAnkylosing spondylitimedicine.anatomical_structureImmunologyImmunohistochemistryFemaleArthritis &amp; Rheumatism
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