Search results for "Th17"

showing 10 items of 97 documents

Dendritic cells tip the balance towards induction of regulatory T cells upon priming in experimental autoimmune encephalomyelitis

2016

Counter-balancing regulatory mechanisms, such as the induction of regulatory T cells (Treg), limit the effects of autoimmune attack in neuroinflammation. However, the role of dendritic cells (DCs) as the most powerful antigen-presenting cells, which are intriguing therapeutic targets in this context, is not fully understood. Here, we demonstrate that conditional ablation of DCs during the priming phase of myelin-specific T cells in experimental autoimmune encephalomyelitis (EAE) selectively aborts inducible Treg (iTreg) induction, whereas generation of T helper (Th)1/17 cells is unaltered. DCs facilitate iTreg induction by creating a milieu with high levels of interleukin (IL)-2 due to a st…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalImmunologyMedizinPriming (immunology)chemical and pharmacologic phenomenaAutoimmunitymedicine.disease_causeLymphocyte ActivationT-Lymphocytes RegulatoryAutoimmunityImmunomodulation03 medical and health sciencesMice0302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betamedicineImmunology and AllergyAnimalsNeuroinflammationCD40biologyMultiple sclerosisExperimental autoimmune encephalomyelitisInterleukinhemic and immune systemsDendritic Cellsmedicine.disease030104 developmental biologyImmunologybiology.proteinInterleukin 12CytokinesTh17 Cells030217 neurology & neurosurgery
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Gatekeeper role of brain antigen‐presenting CD11c + cells in neuroinflammation

2015

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen-presenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c(+) cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+) cells. These CD11c(+) cells are organized in perivascular clusters…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesAntigen-Presenting CellsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInterleukin 210302 clinical medicineCell MovementAnimalsCytotoxic T cellAntigen-presenting cellMolecular BiologyNeuroinflammationInterleukin 3CD40General Immunology and MicrobiologybiologyGeneral NeuroscienceInterleukin-17BrainGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsDendritic CellsArticlesNatural killer T cellCD11c AntigenMice Inbred C57BL030104 developmental biologyImmunologyInterleukin 12biology.proteinTh17 Cells030215 immunologyThe EMBO Journal
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Targeting prohibitins at the cell surface prevents Th17-mediated autoimmunity.

2018

T helper (Th)17 cells represent a unique subset of CD4(+) T cells and are vital for clearance of extracellular pathogens including bacteria and fungi. However, Th17 cells are also involved in orchestrating autoimmunity. By employing quantitative surface proteomics, we found that the evolutionarily conserved prohibitins (PHB1/2) are highly expressed on the surface of both murine and human Th17 cells. Increased expression of PHBs at the cell surface contributed to enhanced CRAF/MAPK activation in Th17 cells. Targeting surface‐expressed PHBs on Th17 cells with ligands such as Vi polysaccharide (Typhim vaccine) inhibited CRAF‐MAPK pathway, reduced interleukin (IL)‐17 expression and ameliorated …

0301 basic medicineMAPK/ERK pathwayMultiple SclerosisT cellCellPopulationAutoimmunityBiologymedicine.disease_causeT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyAutoimmunity03 medical and health sciencesMiceProhibitinsRickettsial VaccinesmedicineAnimalsHumanseducationExtracellular Signal-Regulated MAP KinasesMolecular Biologyeducation.field_of_studyGeneral Immunology and MicrobiologyGeneral NeuroscienceInterleukinFOXP3Forkhead Transcription FactorsArticlesCell biologyRepressor Proteins030104 developmental biologymedicine.anatomical_structureTh17 CellsSignal transductionHeLa CellsSignal TransductionThe EMBO journal
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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Decreased proportions of CD4 + IL17+/CD4 + CD25 + CD127- and CD4 + IL17+/CD4 + CD25 + CD127 - FoxP3+ T cells in children with autoimmune thyroid dise…

2016

Until now, altered balance of Th1 and Th2 immune cells has been postulated to play an important role in the pathogenesis of autoimmune thyroid diseases (AITD). However, recent studies on thyroid diseases have suggested a new role for Th17 cells that have been classified as a new lineage, distinct from Th1, Th2 and Treg cells. Despite wide interest, the role of Th17 cells in the pathogenesis of inflammatory and autoimmune diseases is still debated. The aim of the study was to estimate the proportions of Th17/Treg T cells in peripheral blood from patients with Graves' disease (GD; n = 29, mean age 15.4 ± 5.1 years), Hashimoto's thyroiditis (HT; n = 39, mean age 15.2 ± 4.1 years) and in health…

0301 basic medicineMaleAdolescentGraves' diseaseT cellImmunologychemical and pharmacologic phenomenaHashimoto DiseaseT-Lymphocytes RegulatoryThyroiditisAutoimmune DiseasesImmunophenotyping03 medical and health sciencesYoung Adult0302 clinical medicineImmune systemT-Lymphocyte SubsetsmedicineImmunology and AllergyHumansHashimoto DiseaseLymphocyte CountChildAutoantibodiesbusiness.industryThyroidFOXP3hemic and immune systemsmedicine.diseaseThyroid DiseasesAnti-thyroid autoantibodiesGraves Disease030104 developmental biologymedicine.anatomical_structurePhenotypeCase-Control StudiesImmunologyTh17 CellsFemalebusinessBiomarkers030215 immunologyAutoimmunity
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miR-21 antagonism abrogates Th17 tumor promoting functions in multiple myeloma

2020

Multiple myeloma (MM) is tightly dependent on inflammatory bone marrow microenvironment. IL-17 producing CD4+ T cells (Th17) sustain MM cells growth and osteoclasts-dependent bone damage. In turn, Th17 differentiation relies on inflammatory stimuli. Here, we investigated the role of miR-21 in Th17-mediated MM tumor growth and bone disease. We found that early inhibition of miR-21 in naive T cells (miR-21i-T cells) impaired Th17 differentiation in vitro and abrogated Th17-mediated MM cell proliferation and osteoclasts activity. We validated these findings in NOD/SCID-g-NULL mice, intratibially injected with miR-21i-T cells and MM cells. A Pairwise RNAseq and proteome/phosphoproteome analysis…

0301 basic medicineMaleCancer ResearchBone diseaseApoptosisBone NeoplasmsNodMice SCIDBone NeoplasmT-Lymphocytes RegulatoryTh17 Cell03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationgammopathiesMice Inbred NODmedicineTumor Cells CulturedTumor MicroenvironmentBiomarkers TumorAnimalsHumansMultiple myelomaCell ProliferationChemistryCell growthAnimalApoptosiHematologymedicine.diseasePrognosisXenograft Model Antitumor AssaysIn vitroGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCase-Control StudiesCancer researchTh17 CellsBone marrowAntagonismCase-Control StudieMultiple Myeloma
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Fasciola hepatica reinfection potentiates a mixed Th1/Th2/Th17/Treg response and correlates with the clinical phenotypes of anemia.

2016

Background: Fascioliasis is a severe zoonotic disease of worldwide extension caused by liver flukes. In human fascioliasis hyperendemic areas, reinfection and chronicity are the norm and anemia is the main sign. Herein, the profile of the Th1/Th2/Th17/Treg expression levels is analyzed after reinfection, correlating them with their corresponding hematological biomarkers of morbidity. Methodology/Principal findings: The experimental design reproduces the usual reinfection/chronicity conditions in human fascioliasis endemic areas and included Fasciola hepatica primo-infected Wistar rats (PI) and rats reinfected at 8 weeks (R8), and at 12 weeks (R12), and negative control rats. In a cross-sect…

0301 basic medicineMalePhysiologymedicine.medical_treatmentSnailslcsh:MedicineGene ExpressionImmune PhysiologyGene expressionMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsImmunosuppressionEBI3AnemiaForkhead Transcription FactorsHematologyThymusInterleukin-10Interleukin 10medicine.anatomical_structureHelminth InfectionsCytokinesResearch ArticleNeglected Tropical DiseasesFascioliasisImmunologychemical and pharmacologic phenomenaSpleenBiologyTransforming Growth Factor beta103 medical and health sciencesImmune systemTh2 CellsGeneticsParasitic DiseasesmedicineFasciola hepaticaAnimalsRats WistarCell ProliferationInterleukinslcsh:RBiology and Life SciencesMolecular DevelopmentFasciola hepaticaTh1 CellsTropical Diseasesbiology.organism_classificationRats030104 developmental biologyCross-Sectional StudiesImmune SystemImmunologyTh17 Cellslcsh:QSpleenDevelopmental Biology
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Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
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Ribosome-Targeting Antibiotics Impair T Cell Effector Function and Ameliorate Autoimmunity by Blocking Mitochondrial Protein Synthesis

2019

Summary While antibiotics are intended to specifically target bacteria, most are known to affect host cell physiology. In addition, some antibiotic classes are reported as immunosuppressive for reasons that remain unclear. Here, we show that Linezolid, a ribosomal-targeting antibiotic (RAbo), effectively blocked the course of a T cell-mediated autoimmune disease. Linezolid and other RAbos were strong inhibitors of T helper-17 cell effector function in vitro, showing that this effect was independent of their antibiotic activity. Perturbing mitochondrial translation in differentiating T cells, either with RAbos or through the inhibition of mitochondrial elongation factor G1 (mEF-G1) progressi…

0301 basic medicineMitochondrial translationmedicine.medical_treatmentT-LymphocytesCellMitochondrionmedicine.disease_causeRibosomemitochondrial translationOxidative PhosphorylationantibioticsAutoimmunityACTIVATIONMice0302 clinical medicineribosome-targetingMedicine and Health SciencesImmunology and AllergyTRANSCRIPTION FACTORMolecular Targeted TherapyMice Knockout0303 health sciencesEffectorExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationPeptide Elongation Factor GAnti-Bacterial Agents3. Good healthCell biologymitochondriaInfectious DiseasesCytokinemedicine.anatomical_structureRESPIRATION030220 oncology & carcinogenesisEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisT cellImmunologyINHIBITIONT cellsBiologyOXAZOLIDINONEPeptides CyclicArticleMitochondrial Proteins03 medical and health sciencesNAD+medicineAnimalsHumanselongation factor G1030304 developmental biologyAutoimmune diseaseBacteriaLinezolidBiology and Life SciencesPATHWAYSDNANADmedicine.diseaseIn vitroMice Inbred C57BL030104 developmental biologyTh17 CellsArgyrinCHLORAMPHENICOLMEMBRANERibosomesImmunity
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β1-Integrin– and K(V)1.3 channel–dependent signaling stimulates glutamate release from Th17 cells

2020

Although the impact of Th17 cells on autoimmunity is undisputable, their pathogenic effector mechanism is still enigmatic. We discovered soluble N-ethylmaleimide–sensitive factor attachment receptor (SNARE) complex proteins in Th17 cells that enable a vesicular glutamate release pathway that induces local intracytoplasmic calcium release and subsequent damage in neurons. This pathway is glutamine dependent and triggered by binding of β1-integrin to vascular cell adhesion molecule 1 (VCAM-1) on neurons in the inflammatory context. Glutamate secretion could be blocked by inhibiting either glutaminase or K(V)1.3 channels, which are known to be linked to integrin expression and highly expressed…

0301 basic medicineMultiple SclerosisGlutamic AcidVascular Cell Adhesion Molecule-1Cell Communication03 medical and health sciencesMice0302 clinical medicineAnimalsHumansChannel blockerReceptorNeuroinflammationMice KnockoutKv1.3 Potassium ChannelGlutamate secretionChemistryGlutaminaseCell adhesion moleculeIntegrin beta1Glutamate receptorGeneral MedicineCell biologyGlutamine030104 developmental biology030220 oncology & carcinogenesisTh17 CellsSNARE ProteinsResearch ArticleSignal Transduction
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