2016
Deletion of mTORC1 Activity in CD4+ T Cells Is Associated with Lung Fibrosis and Increased γδ T Cells
Vigeland C, Collins S, Chan-Li Y, Hughes A, Oh M, Powell J, Horton M. Deletion of mTORC1 Activity in CD4+ T Cells Is Associated with Lung Fibrosis and Increased γδ T Cells. PLOS ONE 2016, 11: e0163288. PMID: 27649073, PMCID: PMC5029914, DOI: 10.1371/journal.pone.0163288.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinCD4-Positive T-LymphocytesDisease Models, AnimalInterleukin-17MacrophagesMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutMultiprotein ComplexesNeutrophilsPulmonary FibrosisReceptors, Antigen, T-Cell, gamma-deltaSignal TransductionT-Lymphocyte SubsetsTOR Serine-Threonine KinasesConceptsΓδ T cellsTh17 cellsDevelopment of fibrosisT cellsPulmonary fibrosisIL-17AChronic inflammationCytokines IL-17ADevelopment of bleomycinNovel therapeutic targetLung dysfunctionLung neutrophilsProgressive fibrosisLung fibrosisM2 macrophagesTherapeutic targetFibrosisIncurable diseaseInflammationMortalityBleomycinCellsILCritical rolePrior studies
2012
Epicutaneous Exposure to Staphylococcal Superantigen Enterotoxin B Enhances Allergic Lung Inflammation via an IL-17A Dependent Mechanism
Yu J, Oh MH, Park JU, Myers AC, Dong C, Zhu Z, Zheng T. Epicutaneous Exposure to Staphylococcal Superantigen Enterotoxin B Enhances Allergic Lung Inflammation via an IL-17A Dependent Mechanism. PLOS ONE 2012, 7: e39032. PMID: 22848348, PMCID: PMC3407176, DOI: 10.1371/journal.pone.0039032.Peer-Reviewed Original ResearchConceptsIL-17A-dependent mechanismsAtopic dermatitisAirway hyperresponsivenessAtopic marchLung inflammationDependent mechanismDevelopment of ADSeverity of ADEnterotoxin BSystemic Th2 responseAllergic lung inflammationTh17/ILSkin barrier abnormalitiesIL-6 productionSkin of patientsEpicutaneous exposureAllergic rhinitisIL-17ATh2 responsesEpicutaneous sensitizationLymph nodesImmune environmentLesional skinAllergen ovalbuminStimulating lymphocytes