Search results for "Inducer"

showing 10 items of 178 documents

ILC3 in Axial Spondyloarthritis: the Gut Angle

2019

Purpose of Review: A growing body of evidence supports the relevance of the interleukin-23/interleukin-17 (IL-23/IL-17) pathway for the pathogenesis of axial spondyloarthritis (axSpA) and its treatment. Recently, innate lymphoid cells (ILC), a heterogeneous family of immune effector cells, have been identified as a relevant contributor in tissue homeostasis, partially via IL-23/IL-17 axis. This review describes the biology and the origins of the group 3 ILCs (ILC3s) in humans, focusing on their role in the pathogenesis of axSpA. Recent Findings: Clinical trials showed the effectiveness of IL23/IL-17 axis inhibition in both spondyloarthritis (SpA) and Inflammatory Bowel Disease (IBD). Recent…

0301 basic medicineInterleukin-23Inflammatory bowel diseasePathogenesis03 medical and health sciences0302 clinical medicineRheumatologySpondyloarthritisSpondylarthritismedicineInterleukin 23HumansLymphocytesIL-23/IL-17 axiGut inflammationTissue homeostasisInflammation030203 arthritis & rheumatologyAnkylosing spondylitisInnate immune systembusiness.industryInterleukin-17Innate lymphoid cellLymphoid tissue inducer cellmedicine.diseaseImmunity InnateAnkylosing spondylitiIL-17030104 developmental biologyImmunologyInterleukin 17businessGroup 3 innate lymphoid cellCurrent Rheumatology Reports
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Plasma phospholipid transfer protein (PLTP) modulates adaptive immune functions through alternation of T helper cell polarization

2016

International audience; Objective: Plasma phospholipid transfer protein (PLTP) is a key determinant of lipoprotein metabolism, and both animal and human studies converge to indicate that PLTP promotes atherogenesis and its thromboembolic complications. Moreover, it has recently been reported that PLTP modulates inflammation and immune responses. Although earlier studies from our group demonstrated that PLTP can modify macrophage activation, the implication of PLTP in the modulation of T-cell-mediated immune responses has never been investigated and was therefore addressed in the present study. Approach and results: In the present study, we demonstrated that PLTP deficiency in mice has a pro…

0301 basic medicineLymphocyteIpid Transfer ProteinAdaptive ImmunityCardiovascular-DiseaseT-Lymphocytes RegulatoryLipoprotein MetabolismLeukocyte CountPhospholipid transfer proteinPolarizationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyHypersensitivity DelayedPhospholipid Transfer ProteinsCell PolarityCell DifferentiationT-Lymphocytes Helper-InducerT helper cellFlow CytometryAcquired immune systemCell biologyInfectious Diseasesmedicine.anatomical_structureEndothelial-CellsCytokines[SDV.IMM]Life Sciences [q-bio]/ImmunologyLymphocytemedicine.symptomResearch ArticleDensity-Lipoprotein[SDV.IMM] Life Sciences [q-bio]/ImmunologyHuman Atherosclerotic PlaquesT cellCirculating Interleukin-18ImmunologyT CellAntigen-Presenting CellsInflammationAcute Myocardial-InfarctionGATA3 Transcription FactorBiology03 medical and health sciencesImmune systemmedicineAnimalsAntigen-presenting cellDeficient MiceAlpha-TocopherolMice Inbred C57BL030104 developmental biologyImmunologyVitamin-ET-Box Domain ProteinsBiomarkersSpleen
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miRNA92a targets KLF2 and the phosphatase PTEN signaling to promote human T follicular helper precursors in T1D islet autoimmunity.

2016

Aberrant immune activation mediated by T effector cell populations is pivotal in the onset of autoimmunity in type 1 diabetes (T1D). T follicular helper (TFH) cells are essential in the induction of high-affinity antibodies, and their precursor memory compartment circulates in the blood. The role of TFH precursors in the onset of islet autoimmunity and signaling pathways regulating their differentiation is incompletely understood. Here, we provide direct evidence that during onset of islet autoimmunity, the insulin-specific target T-cell population is enriched with a C-X-C chemokine receptor type 5 (CXCR5)(+)CD4(+) TFH precursor phenotype. During onset of islet autoimmunity, the frequency o…

0301 basic medicineMaleReceptors CXCR5endocrine systemAdolescentPopulationPrimary Cell CultureKruppel-Like Transcription FactorsAutoimmunityMice TransgenicNodBiologymedicine.disease_causeCXCR5Autoimmunity03 medical and health sciencesIslets of LangerhansMicePhosphatidylinositol 3-Kinases0302 clinical medicineMice Inbred NODmedicineAnimalsHumansIL-2 receptorKlf2 ; Pten-pi3k Signaling ; T Follicular Helper Cells ; Mirna92a ; Type 1 DiabeteseducationChildPI3K/AKT/mTOR pathwayNOD miceAutoantibodiesgeographyeducation.field_of_studyMultidisciplinarygeography.geographical_feature_categoryForkhead Box Protein O1PTEN PhosphohydrolaseAntagomirsT-Lymphocytes Helper-InducerIsletMicroRNAs030104 developmental biologyDiabetes Mellitus Type 1Gene Expression RegulationImmunologyCancer researchFemale030215 immunologySignal Transduction
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Nutritional Wheat Amylase-Trypsin Inhibitors Promote Intestinal Inflammation via Activation of Myeloid Cells.

2016

Background & Aims Wheat amylase-trypsin inhibitors (ATIs) are nutritional activators of innate immunity, via activation of the toll-like receptor 4 (TLR4) on myeloid cells. We aimed to characterize the biologic activity of ATIs in various foods and their effect on intestinal inflammation. Methods We selected 38 different gluten-containing and gluten-free products, either unprocessed (such as wheat, rye, barley, quinoa, amaranth, soya, lentils, and rice) or processed (such as pizza, pasta, bread, and biscuits). ATIs were extracted and their biological activities determined in TLR4-responsive mouse and human cell lines. Effects of oral ATIs on intestinal inflammation were determined in health…

0301 basic medicinePharmacologyAdaptive Immunitychemistry.chemical_compoundMice0302 clinical medicineMesenteric lymph nodesMesenteryMyeloid CellsTriticumPlant ProteinsToll-like receptorDextran SulfateGastroenterologyfood and beveragesColitisIntestinesmedicine.anatomical_structureAmylases030211 gastroenterology & hepatologymedicine.symptomTrypsin InhibitorsInterferon InducersGlutensColonDuodenumInflammationIleumBiologyCell Line03 medical and health sciencesDiet Gluten-FreeIleummedicineAnimalsHumansColitisInflammationInnate immune systemHepatologymedicine.diseaseImmunity InnateMice Inbred C57BLToll-Like Receptor 4Celiac Disease030104 developmental biologyPoly I-CchemistryPolyinosinic:polycytidylic acidImmunologyLymph NodesWheat allergyGastroenterology
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Noise-Induced Vascular Dysfunction, Oxidative Stress, and Inflammation Are Improved by Pharmacological Modulation of the NRF2/HO-1 Axis

2021

Vascular oxidative stress, inflammation, and subsequent endothelial dysfunction are consequences of traditional cardiovascular risk factors, all of which contribute to cardiovascular disease. Environmental stressors, such as traffic noise and air pollution, may also facilitate the development and progression of cardiovascular and metabolic diseases. In our previous studies, we investigated the influence of aircraft noise exposure on molecular mechanisms, identifying oxidative stress and inflammation as central players in mediating vascular function. The present study investigates the role of heme oxygenase-1 (HO-1) as an antioxidant response preventing vascular consequences following exposu…

0301 basic medicinePhysiologyClinical BiochemistryInflammationDiseaseRM1-950030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeenvironmental risk factorsBiochemistryArticleendothelial dysfunctionNRF203 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineoxidative stressInducerEndothelial dysfunctionMolecular BiologyDimethyl fumaratebusiness.industryaircraft noise exposureheme oxygenase-1Cell Biologymedicine.diseaseNoise030104 developmental biologychemistryinflammationTherapeutics. Pharmacologymedicine.symptombusinessOxidative stressHeminAntioxidants
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Minimal hepatic encephalopathy is associated with expansion and activation of CD4+CD28−, Th22 and Tfh and B lymphocytes

2017

AbstractPeripheral inflammation acts synergistically with hyperammonemia in inducing neurological alterations in cirrhotic patients with minimal hepatic encephalopathy (MHE). We hypothesized that appearance of MHE would be associated to some specific qualitative change in peripheral inflammation. The aim of this work was to characterize the changes in peripheral inflammation associated to appearance of MHE. We analyzed it by immunophenotyping and cytokine profile analysis, in cirrhotic patients without or with MHE and controls. The main alterations associated specifically with MHE are: 1) increased activation of all subtypes of CD4+ T-lymphocytes, with the increased expression of CD69; 2) i…

0301 basic medicinemedicine.medical_specialtyScienceInflammationArticleMonocytesImmunophenotyping03 medical and health sciencesImmune systemImmunophenotypingCD28 AntigensInternal medicinemedicineHumansCX3CL1Hepatic encephalopathyB-LymphocytesMultidisciplinarybusiness.industryCD69QRCD28HyperammonemiaT-Lymphocytes Helper-Inducermedicine.disease030104 developmental biologyEndocrinologyHepatic EncephalopathyImmunoglobulin GCD4 AntigensImmunologyMedicineCytokinesmedicine.symptombusinesshuman activitiesScientific Reports
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Interleukin-9 and T helper type 9 cells in rheumatic diseases

2016

Summary Interleukin (IL)-9 is a 28-30 kDa monomeric glycosylated polypeptide belonging to the IL-7/IL-9 family of proteins that bind to a composite receptor consisting of the private receptor IL-9R and the IL-2 receptor, gamma (IL-2RG), a common gamma subunit shared by the receptors of many different cytokines. The IL-9R is expressed widely and IL-9 impacts a number of effector cells, such as effector T cells, B cells, innate lymphoid cells, mast cells, polymorphonuclear cells, epithelial cells and smooth muscle cells, playing an important role in regulating inflammatory immunity. The critical role of IL-9 in promoting cellular and humoral immune responses makes it an important focus of pot…

0301 basic medicinerheumatoid arthritispsoriatic arthritisystemic sclerosisSLEReview ArticleIL-9; psoriatic arthritis; rheumatoid arthritis; SLE; systemic sclerosis; Th9 cells; vasculitis; Immunology and Allergy; ImmunologyTh9 cellsvasculitisArthritis RheumatoidInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTh9 cellIL-9; SLE; Th9 cells; psoriatic arthritis; rheumatoid arthritis; systemic sclerosis; vasculitisLupus Erythematosus SystemicMedicineImmunology and AllergyIL-2 receptorpsoriatic arthritisB-LymphocytesInterleukin-17Innate lymphoid cellT-Lymphocytes Helper-InducerAcquired immune systemInterleukin 10vasculitiInterleukin 12systemic sclerosiSignal TransductionImmunologyAutoimmune Diseases03 medical and health sciencesRheumatic DiseasesAnimalsHumans030203 arthritis & rheumatologyScleroderma Systemicbusiness.industryArthritis PsoriaticInterleukin-9rheumatoid arthritiIL-9Immunity HumoralInterleukin 33Settore MED/16 - Reumatologia030104 developmental biologyCTLA-4Immunologybusiness
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Cellular mechanisms of IL-17-induced blood-brain barrier disruption.

2009

Recently T-helper 17 (Th17) cells were demonstrated to disrupt the blood-brain barrier (BBB) by the action of IL-17A. The aim of the present study was to examine the mechanisms that underlie IL-17A-induced BBB breakdown. Barrier integrity was analyzed in the murine brain endothelial cell line bEnd.3 by measuring the electrical resistance values using electrical call impedance sensing technology. Furthermore, in-cell Western blots, fluorescence imaging, and monocyte adhesion and transendothelial migration assays were performed. Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice. IL-17A induced NADPH oxidase- or xanthine oxidase-dependent reactive oxygen species (ROS)…

1303 BiochemistryEncephalomyelitisOccludin10263 Institute of Experimental ImmunologyBiochemistryMice0302 clinical medicineEnzyme InhibitorsCell Line Transformed0303 health sciencesMice Inbred BALB CNADPH oxidasebiologyTight junctionExperimental autoimmune encephalomyelitisInterleukin-17AzepinesT-Lymphocytes Helper-InducerCell biologyEndothelial stem cellBlood-Brain Barrier1305 BiotechnologyBiotechnologyXanthine OxidaseMyosin light-chain kinaseEncephalomyelitis Autoimmune ExperimentalDown-Regulation610 Medicine & healthNaphthalenes03 medical and health sciences1311 GeneticsOccludinGeneticsmedicine1312 Molecular BiologyAnimalsMolecular BiologyMyosin-Light-Chain KinaseNeuroinflammation030304 developmental biologyEndothelial CellsMembrane ProteinsNADPH Oxidasesmedicine.diseaseMolecular biologyAntibodies NeutralizingOxidative Stressbiology.protein570 Life sciences; biologyReactive Oxygen Species030217 neurology & neurosurgeryFASEB journal : official publication of the Federation of American Societies for Experimental Biolog
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RORgamma-expressing Th17 cells induce murine chronic intestinal inflammation via redundant effects of IL-17A and IL-17F.

2008

Background and Aims IL-17–producing CD4 + T-helper cells (Th17) contribute to chronic autoimmune inflammation in the brain, and levels of Th17-derived cytokines increase in patients with colitis, suggesting a role in pathogenesis. We analyzed the roles of Th17 cells and the transcription factor retinoic acid receptor-related organ receptor (ROR)γ, which regulates Th17 differentiation, in chronic intestinal inflammation. Methods Using an adoptive transfer model of colitis, we compared the colitogenic potential of wild-type, interleukin-17A (IL-17A)–, IL-17F–, IL-22–, and RORγ-deficient CD4 + CD25 − T cells in RAG1-null mice. Results Adoptive transfer of IL-17A–, IL-17F–, or IL-22–deficient T…

Adoptive cell transferNeutrophilsReceptors Retinoic Acidmedicine.medical_treatmentBiologyInflammatory bowel diseasePathogenesisMiceInterferonCell MovementmedicineAnimalsIL-2 receptorColitisCells CulturedReceptors Thyroid HormoneHepatologyInterleukinsInterleukin-17GastroenterologyDendritic CellsT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseColitisAdoptive TransferMice Inbred C57BLCytokineImmunologyChronic Diseasebiology.proteinCytokinesAntibodymedicine.drugGastroenterology
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IL28B polymorphisms influence stage of fibrosis and spontaneous or interferon-induced viral clearance in thalassemia patients with hepatitis C virus …

2012

Background. Polymorphisms in the interleukin-28B are important determinants in the spontaneous and drug-induced control of hepatitis C virus infection. Design and Methods. We assessed the association of rs8099917 and rs12979860 polymorphisms with spontaneous viral clearance, severity of liver fibrosis, and response to interferon-monotherapy in 245 Thalassemia Major patients with Hepatitis C Virus infection. Results. Ninety-eight patients (40%) had a spontaneous viral clearance, while 147 patients (60%) developed a chronic infection. Spontaneous viral clearance was more frequent among patients with the T/T genotype of rs8099917 polymorphism (OR 2.130; p=0.008) or C/C genotype of rs12979860 p…

AdultLiver CirrhosisMalethlassemia hepatitis CInterferon InducersAdolescentHepacivirusHepatitis C virusAlpha interferonHepacivirusAdolescent; Adult; Antibodies Viral; Antiviral Agents; Cohort Studies; Female; Follow-Up Studies; Hepacivirus; Hepatitis C Chronic; Humans; Interferon Inducers; Interferon-alpha; Interleukins; Liver Cirrhosis; Male; Polymorphism Single Nucleotide; Prognosis; Viral Load; Young Adult; beta-Thalassemiamedicine.disease_causeAntibodies ViralAntiviral AgentsPolymorphism Single NucleotideCohort StudiesYoung AdultGenotypemedicineHumansInterferon inducerbiologymedicine.diagnostic_testInterleukinsbeta-ThalassemiaInterferon-alphaHematologyHepatitis CHepatitis C ChronicViral Loadbiology.organism_classificationmedicine.diseasePrognosisLiver biopsyImmunologyFemaleInterferonsOriginal Articles and Brief ReportsViral loadFollow-Up Studies
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