2024
Androgen signaling restricts glutaminolysis to drive sex-specific Th17 metabolism in allergic airway inflammation
Chowdhury N, Cephus J, Pilier E, Wolf M, Madden M, Kuehnle S, McKernan K, Jennings E, Arner E, Heintzman D, Chi C, Sugiura A, Stier M, Voss K, Ye X, Scales K, Krystofiak E, Gandhi V, Guzy R, Cahill K, Sperling A, Peebles R, Rathmell J, Newcomb D. Androgen signaling restricts glutaminolysis to drive sex-specific Th17 metabolism in allergic airway inflammation. Journal Of Clinical Investigation 2024, 134: e177242. PMID: 39404231, PMCID: PMC11601904, DOI: 10.1172/jci177242.Peer-Reviewed Original ResearchTh17 cellsAirway inflammationAR signalingT cellsAndrogen receptorTh17-mediated airway inflammationAirway inflammation mouse modelCD4+ T cellsExpression of glutamine transportersCirculating T cellsRegulation of Th17 cellsAllergic airway inflammationCell-mediated diseasesGlutamine uptakeInflammation mouse modelAndrogen signalingMouse modelTh17Increased prevalenceReduced expressionInflammationAndrogenGlutamine transportGlutaminolysisDecreased glutaminolysis
2022
Multiscale 3D genome organization underlies ILC2 ontogenesis and allergic airway inflammation
Michieletto M, Tello-Cajiao J, Mowel W, Chandra A, Yoon S, Joannas L, Clark M, Jimenez M, Wright J, Lundgren P, Williams A, Thaiss C, Vahedi G, Henao-Mejia J. Multiscale 3D genome organization underlies ILC2 ontogenesis and allergic airway inflammation. Nature Immunology 2022, 24: 42-54. PMID: 36050414, PMCID: PMC10134076, DOI: 10.1038/s41590-022-01295-y.Peer-Reviewed Original ResearchConceptsGenome organizationThree-dimensional genome organizationDistal regulatory elementsId2 promoterChromatin accessibilityGenome structureFunction of ILCsTissue homeostasisRegulatory elementsId2 expressionGene expressionIntegrative analysisILC biologyTranscription factor GATA-3Innate lymphoid cellsFunctional differentiationHost defenseAllergic airway inflammationMultiple interactionsMature ILCGATA-3Key roleExpressionAirway inflammationOntogenesis
2021
Targeting In Vivo Metabolic Vulnerabilities of Th2 and Th17 Cells Reduces Airway Inflammation
Healey D, Cephus J, Barone S, Chowdhury N, Dahunsi D, Madden M, Ye X, Yu X, Olszewski K, Young K, Gerriets V, Siska P, Dworski R, Hemler J, Locasale J, Poyurovsky M, Peebles R, Irish J, Newcomb D, Rathmell J. Targeting In Vivo Metabolic Vulnerabilities of Th2 and Th17 Cells Reduces Airway Inflammation. The Journal Of Immunology 2021, 206: 1127-1139. PMID: 33558372, PMCID: PMC7946768, DOI: 10.4049/jimmunol.2001029.Peer-Reviewed Original ResearchMeSH KeywordsAdultAlternariaAnimalsAsthmaBiomarkersBlood GlucoseBronchoalveolar Lavage FluidCase-Control StudiesCells, CulturedDexamethasoneDisease Models, AnimalDrug SynergismFemaleGlucose Transporter Type 1GlutaminaseGlutamineHealthy VolunteersHumansImmunosuppressive AgentsLungMaleMiceMiddle AgedPrimary Cell CulturePyroglyphidaeTh17 CellsTh2 CellsYoung AdultConceptsAirway inflammationHouse dust miteT cellsAsthmatic patientsCytokine productionDust miteIL-17-producing T cellsTh17 CD4 T cellsIL-17-producing cellsT cell cytokine productionPeripheral blood T cellsAllergic airway inflammationT effector cellsCD4 T cellsBronchoalveolar lavage fluidCell cytokine productionInflammatory cytokine productionBlood T cellsLungs of miceGlutamine metabolismAbundant IL-4Glucose transporter 1Airway hyperresponsivenessSteroid therapyEffector cells
2020
An endothelial microRNA-1–regulated network controls eosinophil trafficking in asthma and chronic rhinosinusitis
Korde A, Ahangari F, Haslip M, Zhang X, Liu Q, Cohn L, Gomez JL, Chupp G, Pober JS, Gonzalez A, Takyar SS. An endothelial microRNA-1–regulated network controls eosinophil trafficking in asthma and chronic rhinosinusitis. Journal Of Allergy And Clinical Immunology 2020, 145: 550-562. PMID: 32035607, PMCID: PMC8440091, DOI: 10.1016/j.jaci.2019.10.031.Peer-Reviewed Original ResearchConceptsMiR-1 levelsAllergic airway inflammationChronic rhinosinusitisP-selectin levelsEndothelium-specific overexpressionLung endotheliumAirway eosinophiliaAirway inflammationAsthmatic patientsTissue eosinophiliaMiR-1House dust mite modelEndothelial cellsThymic stromal lymphopoietinNumber of hospitalizationsHuman lung endotheliumIL-13 stimulationCRS cohortQuantitative RT-PCRSputum eosinophiliaAirway obstructionAsthma modelAsthma phenotypesLentiviral vector deliveryMurine model
2016
Allergy-specific Phenome-Wide Association Study for Immunogenes in Turkish Children
Karaca S, Civelek E, Karaca M, Sahiner UM, Ozgul RK, Kocabas CN, Polimanti R, Sekerel BE. Allergy-specific Phenome-Wide Association Study for Immunogenes in Turkish Children. Scientific Reports 2016, 6: 33152. PMID: 27624002, PMCID: PMC5021980, DOI: 10.1038/srep33152.Peer-Reviewed Original ResearchConceptsHypertonic saline challenge testTurkish childrenAllergic airway inflammationPhenome-wide association studySkin prick testRole of immunogeneticsCross-sectional studyDifferent immune functionsAllergic bronchitisCD14 rs2569190Airway inflammationAtopic marchPrick testAsthma diagnosisLung functionBlood testsIL4 rs2243250Immune functionChallenge testAssociation studiesADAM33ComorbiditiesChildrenAssociationAsthma
2014
Treg Cells Expressing the Coinhibitory Molecule TIGIT Selectively Inhibit Proinflammatory Th1 and Th17 Cell Responses
Joller N, Lozano E, Burkett PR, Patel B, Xiao S, Zhu C, Xia J, Tan TG, Sefik E, Yajnik V, Sharpe AH, Quintana FJ, Mathis D, Benoist C, Hafler DA, Kuchroo VK. Treg Cells Expressing the Coinhibitory Molecule TIGIT Selectively Inhibit Proinflammatory Th1 and Th17 Cell Responses. Immunity 2014, 40: 569-581. PMID: 24745333, PMCID: PMC4070748, DOI: 10.1016/j.immuni.2014.02.012.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell ProliferationCells, CulturedCytokinesEosinophilsFibrinogenForkhead Transcription FactorsGene Expression ProfilingGene Expression RegulationImmunosuppression TherapyLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicReceptors, ImmunologicRespiratory HypersensitivityT-Lymphocyte SubsetsT-Lymphocytes, RegulatoryTh1-Th2 BalanceConceptsTreg cell subsetsTh2 cell responsesTreg cellsCell subsetsCell responsesProinflammatory T helper 1T effector cell proliferationTreg cell-mediated suppressionFibrinogen-like protein 2Allergic airway inflammationT regulatory (Treg) cellsTh2 cytokine productionSuppression of Th1T helper 1Effector cell proliferationTreg signature genesProinflammatory Th1TIGIT expressionAirway inflammationTh17 cellsRegulatory cellsHelper 1Cytokine productionT cellsImmune response
2013
Short Palate, Lung, and Nasal Epithelial Clone–1 Is a Tightly Regulated Airway Sensor in Innate and Adaptive Immunity
Britto CJ, Liu Q, Curran DR, Patham B, Dela Cruz CS, Cohn L. Short Palate, Lung, and Nasal Epithelial Clone–1 Is a Tightly Regulated Airway Sensor in Innate and Adaptive Immunity. American Journal Of Respiratory Cell And Molecular Biology 2013, 48: 717-724. PMID: 23470624, PMCID: PMC3727874, DOI: 10.1165/rcmb.2012-0072oc.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAnimalsCell Line, TumorGene Expression RegulationGlycoproteinsHumansImmunity, InnateImmunohistochemistryInflammationInfluenza A virusInterferon-gammaLipopolysaccharidesLungMiceMice, Inbred C57BLPhosphoproteinsPneumonia, BacterialPseudomonas aeruginosaRespiratory MucosaRespiratory Tract InfectionsStreptococcus pneumoniaeConceptsNasal epithelial clone 1Lower respiratory tractRespiratory tractAirway inflammationShort palateTh2-induced airway inflammationHost defenseAllergic airway inflammationCommon respiratory pathogensAirway epithelial cellsModel of pneumoniaAirway surface liquidPathogen-associated molecular patternsGreatest environmental exposureClone 1Mucociliary clearanceRespiratory pathogensAirway sensorsRespiratory epitheliumAdaptive immunitySPLUNC1IFN-γ actBasal conditionsMRNA expressionMolecular patterns
2011
IFN-γ Acts on the Airway Epithelium To Inhibit Local and Systemic Pathology in Allergic Airway Disease
Mitchell C, Provost K, Niu N, Homer R, Cohn L. IFN-γ Acts on the Airway Epithelium To Inhibit Local and Systemic Pathology in Allergic Airway Disease. The Journal Of Immunology 2011, 187: 3815-3820. PMID: 21873527, PMCID: PMC3178669, DOI: 10.4049/jimmunol.1100436.Peer-Reviewed Original ResearchConceptsAirway epitheliumAllergic airway inflammationAllergic airway diseaseTh2 cell activationGoal of therapyProduction of IFNAdministration of medicationsSystemic side effectsAirway mucosal surfaceAirway epithelial cellsSites of inflammationIFN-γ actionAirway inflammationAirway obstructionPersistent asthmaRefractory asthmaAirway diseaseIFN-γRTh1 cellsPathological responseSystemic pathologyEffector functionsSide effectsBone marrowAsthma
2010
Cell-permeable Foxp3 protein alleviates autoimmune disease associated with inflammatory bowel disease and allergic airway inflammation
Choi JM, Shin JH, Sohn MH, Harding MJ, Park JH, Tobiasova Z, Kim DY, Maher SE, Chae WJ, Park SH, Lee CG, Lee SK, Bothwell AL. Cell-permeable Foxp3 protein alleviates autoimmune disease associated with inflammatory bowel disease and allergic airway inflammation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 18575-18580. PMID: 20937878, PMCID: PMC2972952, DOI: 10.1073/pnas.1000400107.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAsthmaAutoimmune DiseasesCell Membrane PermeabilityDisease Models, AnimalFemaleForkhead Transcription FactorsHumansInflammatory Bowel DiseasesLymphocyte ActivationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsRecombinant Fusion ProteinsT-Lymphocytes, RegulatoryConceptsAllergic airway inflammationT cellsAirway inflammationAllergic diseasesFOXP3 proteinOvalbumin-induced allergic airway inflammationWild-type CD4 T cellsAllergic disease modelsDevelopment of colitisInflammatory bowel diseaseRegulatory T cellsCD4 T cellsInflammatory immune responseT cell activationFoxP3 transductionBowel diseaseScurfy miceTreg functionAutoimmune diseasesAutoimmune symptomsIntranasal deliveryTherapeutic effectImmune responseSystemic deliveryClinical potentialAirway epithelium response to IFN-γ regulates allergic airway inflammation (91.7)
Mitchell C, Provost K, Niu N, Homer R, Cohn L. Airway epithelium response to IFN-γ regulates allergic airway inflammation (91.7). The Journal Of Immunology 2010, 184: 91.7-91.7. DOI: 10.4049/jimmunol.184.supp.91.7.Peer-Reviewed Original ResearchAirway epithelial cellsAllergic airway inflammationAllergic airway diseaseAirway eosinophiliaAirway inflammationAirway diseaseNon-hematopoietic cellsEpithelial cellsIFN-γRIFN-γ receptor-deficient miceIFN-γR expressionReceptor-deficient miceBone marrow chimerasOVA-specific Th1Th1 cellsDeficient miceMucus productionBone marrowEpithelium responseIFNMaximal inhibitionEosinophiliaInflammationMiceInhibitory effect
2009
Regulation of Immature Dendritic Cell Migration by RhoA Guanine Nucleotide Exchange Factor Arhgef5*
Wang Z, Kumamoto Y, Wang P, Gan X, Lehmann D, Smrcka AV, Cohn L, Iwasaki A, Li L, Wu D. Regulation of Immature Dendritic Cell Migration by RhoA Guanine Nucleotide Exchange Factor Arhgef5*. Journal Of Biological Chemistry 2009, 284: 28599-28606. PMID: 19713215, PMCID: PMC2781403, DOI: 10.1074/jbc.m109.047282.Peer-Reviewed Original ResearchConceptsDendritic cellsBone marrow-derived mature dendritic cellsMigration of DCsAllergic airway inflammationImmature dendritic cellsMature dendritic cellsDendritic cell migrationRAW264.7 cell lineHuman embryonic kidney 293 cellsAirway inflammationShort hairpin RNALymph nodesEmbryonic kidney 293 cellsB lymphocytesActivation of RhoALeukocyte chemotaxisKidney 293 cellsMouse linesMouse macrophagesHairpin RNACell linesVivo roleCell migrationChemotaxisARHGEF5Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation
Niu N, Laufer T, Homer RJ, Cohn L. Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation. The Journal Of Immunology 2009, 183: 1523-1527. PMID: 19596982, DOI: 10.4049/jimmunol.0901349.Peer-Reviewed Original ResearchConceptsAllergic airway inflammationMHC class II expressionAirway inflammationDendritic cellsClass II expressionTh2 generationTh2 immunityTh2-dependent allergic airway inflammationTh1 immune responseIFN-gamma productionAirway neutrophiliaTh2 primingRespiratory tractTh2 cellsImmune responseClass II signalsInflammationTh2 recruitmentMice resultsMiceCells altersImmunityActivationCellsNeutrophiliaDecreased Ovalbumin‐induced Airway Inflammation in Mice Deficient in the Sensory Neuronal Ion Channel TRPA1
Caceres A, Brackmann M, Bessac B, Cohn L, Jordt S. Decreased Ovalbumin‐induced Airway Inflammation in Mice Deficient in the Sensory Neuronal Ion Channel TRPA1. The FASEB Journal 2009, 23: 580.10-580.10. DOI: 10.1096/fasebj.23.1_supplement.580.10.Peer-Reviewed Original ResearchChronic obstructive pulmonary diseaseAirway inflammationOvalbumin-induced airway inflammationOvalbumin mouse modelAllergic airway inflammationObstructive pulmonary diseaseTRPA1-deficient miceChronic inflammatory statePeripheral sensory neuronsBronchoalveolar lavage fluidPro-inflammatory peptidesTh2-derived cytokinesIon channel TRPA1Lipid peroxidation productsAirway conditionsEosinophil infiltrationInflammatory mediatorsPulmonary diseaseNeuronal releaseAirway constrictionInflammatory stateLavage fluidVascular leakageEdema formationInflammatory process
2001
IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation
Cohn L, Herrick C, Niu N, Homer R, Bottomly K. IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation. The Journal Of Immunology 2001, 166: 2760-2767. PMID: 11160342, DOI: 10.4049/jimmunol.166.4.2760.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, CutaneousAdministration, IntranasalAdoptive TransferAnimalsBone Marrow CellsBone Marrow TransplantationBronchiCell MovementDown-RegulationEosinophilsFemaleHematopoietic Stem CellsInflammationInterferon-gammaInterleukin-13Interleukin-4Interleukin-5MaleMiceMice, Inbred BALB CMice, KnockoutMice, TransgenicOvalbuminPulmonary EosinophiliaReceptors, InterferonRespiratory HypersensitivityTh2 CellsUp-RegulationConceptsAirway eosinophiliaIL-4IFN-gammaTh2 cellsAirway eosinophilsIL-5Allergic airway inflammationIFN-γ productionTh2 cell generationAirway inflammationEosinophilic inflammationLung eosinophiliaLung parenchymalTh2 cytokinesIntranasal administrationRespiratory tractLung tissueCounterregulatory effectsEosinophiliaCell transferEosinophilsHemopoietic cellsInflammationAirwayIFNA critical role for NF-κB in Gata3 expression and TH2 differentiation in allergic airway inflammation
Das J, Chen C, Yang L, Cohn L, Ray P, Ray A. A critical role for NF-κB in Gata3 expression and TH2 differentiation in allergic airway inflammation. Nature Immunology 2001, 2: 45-50. PMID: 11135577, DOI: 10.1038/83158.Peer-Reviewed Original ResearchConceptsAllergic airway inflammationT helper 2GATA-3 expressionTh2 differentiationAirway inflammationGATA3 expressionAirway eosinophilic inflammationTh2 cytokine productionT-bet expressionInterferon-γ ProductionTh2 cell recruitmentTranscription factor GATA-3NF-κB activityNuclear factor κBT cell receptorEosinophilic inflammationHelper 2Asthma pathogenesisCytokine productionIL-13IL-5Th2 cellsT cellsInterleukin-4Cell recruitment
1999
T Helper 1 Cells and Interferon γ Regulate Allergic Airway Inflammation and Mucus Production
Cohn L, Homer R, Niu N, Bottomly K. T Helper 1 Cells and Interferon γ Regulate Allergic Airway Inflammation and Mucus Production. Journal Of Experimental Medicine 1999, 190: 1309-1318. PMID: 10544202, PMCID: PMC2195688, DOI: 10.1084/jem.190.9.1309.Peer-Reviewed Original ResearchConceptsTh1 cellsTh2 cellsMucus productionAirway eosinophiliaIFN-gammaRecipient miceAirway inflammationIFN-gamma receptor signalingT helper type 1T helper 1 cellsAllergic airway inflammationTh2 cytokine secretionHelper type 1Different inhibitory pathwaysAsthmatic patientsPathologic featuresCytokine secretionInflammatory responseRespiratory tractEosinophiliaInhibitory pathwaysMouse modelInflammationType 1Marked reduction
1998
Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
Yang L, Cohn L, Zhang D, Homer R, Ray A, Ray P. Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation. Journal Of Experimental Medicine 1998, 188: 1739-1750. PMID: 9802985, PMCID: PMC2212522, DOI: 10.1084/jem.188.9.1739.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigensAsthmaBase SequenceChemokine CCL11Chemokines, CCCytokinesDNA PrimersEosinophiliaGene ExpressionInflammationIntercellular Adhesion Molecule-1Interleukin-4Interleukin-5LungMiceMice, Inbred C57BLMice, KnockoutNF-kappa BNF-kappa B p50 SubunitOvalbuminReverse Transcriptase Polymerase Chain ReactionTh2 CellsVascular Cell Adhesion Molecule-1ConceptsAirway inflammationEosinophil-rich airway inflammationTh2 cytokine interleukin-5Adhesion molecules VCAM-1Chemokine macrophage inflammatory proteinCell adhesion molecule VCAM-1Allergic airway inflammationEosinophilic airway inflammationT cell primingPathogenesis of asthmaT helper 2T cell recruitmentInduction of eosinophiliaMacrophage inflammatory proteinCytokines interleukin-5Wild-type miceSites of inflammationNuclear factor κBAllergic asthmaAsthmatic airwaysHelper 2Cell primingInflammatory proteinMIP-1betaExtravasation of eosinophils
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply