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dc.rights.licenseopenen_US
dc.contributor.authorGUTTMAN-YASSKY, E.
dc.contributor.authorFACHERIS, P.
dc.contributor.authorGOMEZ-ARIAS, P.J.
dc.contributor.authorDEL DUCA, E.
dc.contributor.authorDA ROSA, J.C.
dc.contributor.authorWEIDINGER, S.
dc.contributor.authorBISSONNETTE, R.
dc.contributor.authorARMSTRONG, A.W.
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
dc.contributor.authorSENESCHAL, Julien
dc.contributor.authorEYERICH, K.
dc.contributor.authorESTRADA, Y.D.
dc.contributor.authorBOSE, S.N.
dc.contributor.authorXU, D.
dc.contributor.authorCHEN, A.
dc.contributor.authorTATULYCH, S.
dc.contributor.authorGÜLER, E.
dc.contributor.authorCHAN, G.
dc.contributor.authorPAGE, K.M.
dc.contributor.authorKERKMANN, U.
dc.date.accessioned2024-09-26T09:24:42Z
dc.date.available2024-09-26T09:24:42Z
dc.date.issued2023
dc.identifier.issn0105-4538en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/201839
dc.description.abstractEnBackground: This is the first report on the effects of abrocitinib, a Janus kinase 1–selective inhibitor, on the expression of skin biomarkers in patients with moderate-to-severe atopic dermatitis (AD). Methods: JADE MOA (NCT03915496) was a double-blind Phase 2a trial. Adults were randomly assigned 1:1:1 to receive monotherapy with once-daily abrocitinib 200 mg, abrocitinib 100 mg, or placebo for 12 weeks. The primary endpoint was change from baseline in markers of inflammation (matrix metalloproteinase [MMP]-12), epidermal hyperplasia (keratin-16 [KRT16]), T-helper 2 (Th2) immune response (C-C motif chemokine ligand [CCL]17, CCL18, and CCL26), and Th22 immune response (S100 calcium binding protein A8, A9, and A12 [S100A8, S100A9, and S100A12]) in skin through 12 weeks. Results: A total of 46 patients received abrocitinib 200 mg (n = 14), abrocitinib 100 mg (n = 16), or placebo (n = 16). Abrocitinib improved AD clinical signs and reduced itch. Gene expression of MMP-12, KRT16, S100A8, S100A9, and S100A12 was significantly decreased from baseline with abrocitinib 200 mg (at Weeks 2, 4, and 12) and abrocitinib 100 mg (at Weeks 4 and 12) in a dose-dependent manner. Abrocitinib 200 mg resulted in significant decreases from baseline in CCL17 expression at Week 12 and CCL18 expression at Weeks 2, 4, and 12; no significant decreases were observed for CCL26. Conclusions: Alongside improvements in clinical signs and symptoms of AD, 12 weeks of abrocitinib treatment resulted in downregulation of genes associated with inflammation, epidermal hyperplasia, and Th2 and Th22 immune responses in the skin of patients with moderate-to-severe AD.
dc.language.isoENen_US
dc.rightsAttribution-NonCommercial 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/us/*
dc.subject.enAtopic dermatitis
dc.subject.enBiomarkers
dc.subject.enDermatology
dc.title.enEffect of abrocitinib on skin biomarkers in patients with moderate-to-severe atopic dermatitis
dc.typeArticle de revueen_US
dc.identifier.doi10.1111/all.15969en_US
dc.subject.halSciences du Vivant [q-bio]/Immunologieen_US
dc.identifier.pubmed38108208en_US
bordeaux.journalAllergyen_US
bordeaux.hal.laboratoriesImmunoConcEpT - UMR 5164en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-04710292
hal.version1
hal.date.transferred2024-09-26T09:24:46Z
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
dc.rights.ccCC BY-NCen_US
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