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
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