2017
Expression of IL-22 in the Skin Causes Th2-Biased Immunity, Epidermal Barrier Dysfunction, and Pruritus via Stimulating Epithelial Th2 Cytokines and the GRP Pathway
Lou H, Lu J, Choi EB, Oh MH, Jeong M, Barmettler S, Zhu Z, Zheng T. Expression of IL-22 in the Skin Causes Th2-Biased Immunity, Epidermal Barrier Dysfunction, and Pruritus via Stimulating Epithelial Th2 Cytokines and the GRP Pathway. The Journal Of Immunology 2017, 198: 2543-2555. PMID: 28228560, PMCID: PMC5360537, DOI: 10.4049/jimmunol.1600126.Peer-Reviewed Original ResearchConceptsGastrin-releasing peptideType 2 cytokinesAtopic dermatitisIL-22GRP receptorAD skinDevelopment of ADPathogenesis of ADExpression of GRPHouse dust mite allergenDermal immune cellsIntensity of pruritusAD-like phenotypeThymic stromal lymphopoietinCytokine IL-22Human atopic dermatitisSystemic immune responsesEpidermal barrier dysfunctionImportant pathogenic roleTh2-biased immunitySkin of patientsDust mite allergenSkin of miceChronic pruritic dermatitisAllergen exposure
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
2013
TRPA1-Dependent Pruritus in IL-13–Induced Chronic Atopic Dermatitis
Oh MH, Oh SY, Lu J, Lou H, Myers AC, Zhu Z, Zheng T. TRPA1-Dependent Pruritus in IL-13–Induced Chronic Atopic Dermatitis. The Journal Of Immunology 2013, 191: 5371-5382. PMID: 24140646, PMCID: PMC4175413, DOI: 10.4049/jimmunol.1300300.Peer-Reviewed Original ResearchMeSH KeywordsAcetanilidesAnimalsCalcium ChannelsCells, CulturedChronic DiseaseCytokinesDermatitis, AtopicDisease Models, AnimalHumansInterleukin-13Mast CellsMiceMice, Inbred C57BLMice, TransgenicNerve FibersNerve Tissue ProteinsNeuropeptidesPruritusPurinesTh1-Th2 BalanceTransient Receptor Potential ChannelsTRPA1 Cation ChannelUp-RegulationConceptsTransient receptor potential ankyrin 1Chronic atopic dermatitisAtopic dermatitisMast cellsChronic itchTRPA1 expressionAfferent nervesIL-13Nerve fibersInhibition of TRPA1Histamine-independent itchSensory nerve fibersAfferent nerve fibersDorsal root gangliaNovel neural mechanismAD skinAD miceItch pathwaysLesional skinRoot gangliaInflammatory environmentHealthy subjectsSpecific antagonistMouse modelAnkyrin 1