2019
Effector TH17 Cells Give Rise to Long-Lived TRM Cells that Are Essential for an Immediate Response against Bacterial Infection
Vesely M, Pallis P, Bielecki P, Low JS, Zhao J, Harman CCD, Kroehling L, Jackson R, Bailis W, Licona-Limón P, Xu H, Iijima N, Pillai PS, Kaplan DH, Weaver CT, Kluger Y, Kowalczyk MS, Iwasaki A, Pereira JP, Esplugues E, Gagliani N, Flavell RA. Effector TH17 Cells Give Rise to Long-Lived TRM Cells that Are Essential for an Immediate Response against Bacterial Infection. Cell 2019, 178: 1176-1188.e15. PMID: 31442406, PMCID: PMC7057720, DOI: 10.1016/j.cell.2019.07.032.Peer-Reviewed Original ResearchConceptsCD4 TTissue-resident memory T cellsBacterial infectionsResident memory T cellsFunction of airwayLife-long protectionEffector memory TMemory T cellsTh17 cellsTRM cellsΓδ TEffector cellsMemory TBacterial clearanceT cellsIL-7Adaptive immunityMouse modelMemory responsesVaccine designHost defenseLymphatic endothelial cellsDepletion studiesEndothelial cellsCellular origin
2017
Intestinal type 1 regulatory T cells migrate to periphery to suppress diabetogenic T cells and prevent diabetes development
Yu H, Gagliani N, Ishigame H, Huber S, Zhu S, Esplugues E, Herold KC, Wen L, Flavell RA. Intestinal type 1 regulatory T cells migrate to periphery to suppress diabetogenic T cells and prevent diabetes development. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: 10443-10448. PMID: 28894001, PMCID: PMC5625908, DOI: 10.1073/pnas.1705599114.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsCell- and Tissue-Based TherapyCell DifferentiationCell MovementCell ProliferationDiabetes Mellitus, Type 1DysbiosisFemaleGastrointestinal MicrobiomeImmune ToleranceInterleukin-10IntestinesMiceMice, Inbred NODMice, KnockoutReceptors, CCR4Receptors, CCR5Receptors, CCR7T-Lymphocytes, RegulatoryConceptsRegulatory T cellsTr1 cellsT cellsIL-10-producing type 1 regulatory T cellsType 1 regulatory T cellsAntigen-specific Tr1 cellsGut-associated lymphoid tissueDouble reporter miceDiabetogenic T cellsEffector T cellsDevelopment of diabetesT cells migrateIL-10 signalingType 1 diabetes managementIL-10R.NOD miceIL-10Diabetes incidenceDiabetes developmentAutoimmune diseasesTCR transgenicTh1 cellsLymphoid tissueChemokine receptorsPreclinical models
2015
Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation
Gagliani N, Vesely M, Iseppon A, Brockmann L, Xu H, Palm NW, de Zoete MR, Licona-Limón P, Paiva RS, Ching T, Weaver C, Zi X, Pan X, Fan R, Garmire LX, Cotton MJ, Drier Y, Bernstein B, Geginat J, Stockinger B, Esplugues E, Huber S, Flavell RA. Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation. Nature 2015, 523: 221-225. PMID: 25924064, PMCID: PMC4498984, DOI: 10.1038/nature14452.Peer-Reviewed Original ResearchConceptsRegulatory T cellsResolution of inflammationInflammatory diseasesT cellsTh17 cellsImmune responseT helper cell typeTherapeutic opportunitiesAnti-inflammatory fateT helper cellsAnti-inflammatory phenotypeHuman inflammatory diseasesBeneficial host responseAryl hydrocarbon receptorIL-17ARegulatory cellsHelper cellsSignature cytokinesMouse modelTranscriptional profilesHost responseInflammationCytokinesHydrocarbon receptorDisease
2012
Effector CD4+ T Cell Expression Signatures and Immune-Mediated Disease Associated Genes
Zhang W, Ferguson J, Ng SM, Hui K, Goh G, Lin A, Esplugues E, Flavell RA, Abraham C, Zhao H, Cho JH. Effector CD4+ T Cell Expression Signatures and Immune-Mediated Disease Associated Genes. PLOS ONE 2012, 7: e38510. PMID: 22715389, PMCID: PMC3371029, DOI: 10.1371/journal.pone.0038510.Peer-Reviewed Original ResearchConceptsDifferential gene expressionGenome-wide association studiesGene expressionCell differentiationDisease locusT cell differentiationExpression signaturesDifferential regulation patternsDisease association signalsDisease-associated genesPromoter methylation studiesGenomic lociTransmembrane domainRegulation patternsFunctional pathwaysAssociation studiesMethylation studiesAssociated geneAbundant isoformGenesLociMolecular resolutionPromoter methylationRNAseqCritical role
2011
Development of Autoimmune Diabetes in the Absence of Detectable IL-17A in a CD8-Driven Virally Induced Model
Van Belle TL, Esplugues E, Liao J, Juntti T, Flavell RA, von Herrath MG. Development of Autoimmune Diabetes in the Absence of Detectable IL-17A in a CD8-Driven Virally Induced Model. The Journal Of Immunology 2011, 187: 2915-2922. PMID: 21832162, PMCID: PMC3169711, DOI: 10.4049/jimmunol.1000180.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell SeparationDiabetes Mellitus, Type 1Disease Models, AnimalFemaleFlow CytometryGene Knock-In TechniquesGenes, ReporterGreen Fluorescent ProteinsInterleukin-17Lymphocytic choriomeningitis virusMaleMiceMice, Inbred C57BLVirus DiseasesConceptsType 1 diabetesIL-17AIL-17IL-17A.T cellsViral infectionAutoimmune diabetes developmentVirus-induced modelIL-17 levelsIL-17A productionΓδ T cellsLymphocytic choriomeningitis virusAutoimmune diabetesAutoimmune disordersChronic inflammationDiabetes developmentViral eliminationReporter miceDiabetesBacterial infectionsInfectionCD8Recent studiesCellsInflammationControl of TH17 cells occurs in the small intestine
Esplugues E, Huber S, Gagliani N, Hauser AE, Town T, Wan YY, O’Connor W, Rongvaux A, Van Rooijen N, Haberman AM, Iwakura Y, Kuchroo VK, Kolls JK, Bluestone JA, Herold KC, Flavell RA. Control of TH17 cells occurs in the small intestine. Nature 2011, 475: 514-518. PMID: 21765430, PMCID: PMC3148838, DOI: 10.1038/nature10228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesCD3 ComplexCD4-Positive T-LymphocytesCell MovementChemokine CCL20Disease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression ProfilingGene Expression RegulationInfluenza A virusInterleukin-17Intestine, SmallMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicOrthomyxoviridae InfectionsReceptors, CCR6SepsisStaphylococcal InfectionsTh17 CellsConceptsTh17 cellsImmune systemSmall intestineCD3-specific antibodiesT helper cellsModel of sepsisNumerous autoimmune diseasesRheumatoid arthritisMultiple sclerosisAutoimmune diseasesHelper cellsGastrointestinal tractViral infectionIntestineCellsSepsisTh17ArthritisSclerosisPathogenesisInfectionInfluenzaDiseaseMiceTract
2004
Identification and characterization of a novel spliced variant that encodes human soluble tumor necrosis factor receptor 2
Lainez B, Fernandez-Real J, Romero X, Esplugues E, Cañete J, Ricart W, Engel P. Identification and characterization of a novel spliced variant that encodes human soluble tumor necrosis factor receptor 2. International Immunology 2004, 16: 169-177. PMID: 14688072, DOI: 10.1093/intimm/dxh014.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAlternative SplicingAnimalsArthritis, RheumatoidBase SequenceChlorocebus aethiopsCloning, MolecularCOS CellsEnzyme-Linked Immunosorbent AssayEtanerceptFemaleHumansImmunoglobulin GMaleMiddle AgedMolecular Sequence DataProtein IsoformsReceptors, Tumor Necrosis FactorSepsisTransfectionTumor Necrosis Factor-alphaConceptsAlternative splicingCell death inductionTNF-alpha-induced apoptosisExtracellular ectodomainMultiple inflammatory pathologiesCytoplasmic domainNovel isoformHuman TNFR2COS cellsExpression studiesDeath inductionCell typesTNF-alpha functionReceptors TNFR1SplicingExon 7Soluble formIsoformsBiological effectsBiological activityTumor necrosis factor receptor 2Pleiotropic cytokineNecrosis factor receptor 2Factor receptor 2TNFR2