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 exposureA novel multi-network approach reveals tissue-specific cellular modulators of fibrosis in systemic sclerosis
Taroni JN, Greene CS, Martyanov V, Wood TA, Christmann RB, Farber HW, Lafyatis RA, Denton CP, Hinchcliff ME, Pioli PA, Mahoney JM, Whitfield ML. A novel multi-network approach reveals tissue-specific cellular modulators of fibrosis in systemic sclerosis. Genome Medicine 2017, 9: 27. PMID: 28330499, PMCID: PMC5363043, DOI: 10.1186/s13073-017-0417-1.Peer-Reviewed Original ResearchConceptsDisease-associated signaturesFunctional genomic networksGene expression signaturesPulmonary fibrosisAutoimmune diseasesDisease processMulti-organ autoimmune diseaseDistinct underlying pathologyPro-fibrotic macrophagesInternal organ involvementPulmonary arterial hypertensionExpression signaturesSkin of patientsInnate immune systemWilcoxon rank sum testGenomic networksRank sum testBackgroundSystemic sclerosisArterial hypertensionOrgan involvementSystemic sclerosisUnderlying pathologyLung microenvironmentSkin fibrosisFibrotic genesCOL6A5 variants in familial neuropathic chronic itch
Martinelli-Boneschi F, Colombi M, Castori M, Devigili G, Eleopra R, Malik RA, Ritelli M, Zoppi N, Dordoni C, Sorosina M, Grammatico P, Fadavi H, Gerrits MM, Almomani R, Faber CG, Merkies IS, Toniolo D, Network F, Cocca M, Doglioni C, Waxman S, Dib-Hajj S, Taiana M, Sassone J, Lombardi R, Cazzato D, Zauli A, Santoro S, Marchi M, Lauria G. COL6A5 variants in familial neuropathic chronic itch. Brain 2017, 140: 555-567. PMID: 28073787, DOI: 10.1093/brain/aww343.Peer-Reviewed Original ResearchConceptsChronic itchSmall fiber neuropathyJHS/EDS-HT patientsJoint hypermobility syndrome/Ehlers-Danlos syndrome hypermobility typeNew candidate therapeutic targetsIntraepidermal nerve fiber densityEhlers-Danlos syndrome hypermobility typeEDS-HT patientsNonsense variantNerve fiber densitySkin of patientsCandidate therapeutic targetUnrelated sporadic patientsWhole-exome sequencingItch reliefNeuropathic itchDiabetic patientsHypermobility typeSomatosensory pathwaysHealthy controlsSkin biopsiesSide effectsTherapeutic targetPatientsSporadic patients
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
1993
Altered Metabolism of Mast-Cell Growth Factor (c-kit Ligand) in Cutaneous Mastocytosis
Longley B, Morganroth G, Tyrrell L, Ding T, Anderson D, Williams D, Halaban R. Altered Metabolism of Mast-Cell Growth Factor (c-kit Ligand) in Cutaneous Mastocytosis. New England Journal Of Medicine 1993, 328: 1302-1307. PMID: 7682288, DOI: 10.1056/nejm199305063281803.Peer-Reviewed Original ResearchConceptsMast cell growth factorMessenger RNAGrowth factorC-kit proto-oncogeneProduction of melaninSoluble formGrowth factor geneFactor genesProteolytic processingProto-oncogeneSequence abnormalitiesExtracellular spaceAltered metabolismAltered distributionGrowth factor messenger RNASkin of patientsDermal cellsCellsPolymerase chain reactionCutaneous mastocytosisMast cells
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