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The role of interleukin-17 in mouse models of atopic dermatitis and contact dermatitis

DC FieldValueLanguage
dc.contributor.author손명현-
dc.contributor.author오미선-
dc.contributor.author홍정연-
dc.contributor.author김경원-
dc.contributor.author김규언-
dc.contributor.author김미나-
dc.contributor.author김윤선-
dc.date.accessioned2016-02-04T11:39:59Z-
dc.date.available2016-02-04T11:39:59Z-
dc.date.issued2015-
dc.identifier.issn0307-6938-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/140929-
dc.description.abstractBACKGROUND: Atopic dermatitis (AD) and contact dermatitis (CD) are both T cell-mediated eczematous disorders. Interleukin (IL)-17, expressed by T helper (Th)17 cells, is involved in recruitment of inflammatory cells into AD and CD skin. AIM: In this study, we investigated whether IL-17 regulates immune dysregulation and affects skin barrier in oxazolone (OXA)-induced AD-like and CD-like disease models in mice, by comparing IL-17 null mutant (IL-17(-/-) ) vs. wild-type (WT) mouse strains in the models. METHODS: IL-17(-/-) and WT Balb/c mice were used for OXA induction of AD-like and CD-like skin diseases. Ear swelling was measured by a micrometer. Skin biopsies were obtained for RNA isolation and histology. Real-time quantitative PCR analysis was performed to quantify mRNA expression of Th2 cytokines. Skin permeability was measured by a vapometer, and structural changes in the skin were evaluated by electron and confocal microscopy. RESULTS: Both OXA-induced AD and CD responses were alleviated in IL-17(-/-) mice relative to WT, as demonstrated by reductions in ear swelling, inflammatory cell infiltration and levels of Th2 cytokines. These endpoints were used to characterize inflammatory dysregulation in both AD and CD models. Skin-barrier dysfunction, measured by increases in transepidermal water loss and dysfunction of lamellar bodies, and reductions in lipid distribution, were seen in both AD and CD in WT mice. In IL-17(-/-) mice, however, these responses were significantly diminished. CONCLUSIONS: The results indicate that the IL-17 gene may play a role in modulating immune dysregulation and affecting skin barrier in OXA-induced AD-like and CD-like skin disease models in the Balb/c mouse.-
dc.description.statementOfResponsibilityopen-
dc.format.extent665~671-
dc.relation.isPartOfClinical and Experimental Dermatology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCytokines/metabolism-
dc.subject.MESHDermatitis, Atopic/immunology*-
dc.subject.MESHDermatitis, Atopic/metabolism-
dc.subject.MESHDermatitis, Atopic/pathology-
dc.subject.MESHDermatitis, Contact/immunology*-
dc.subject.MESHDermatitis, Contact/metabolism-
dc.subject.MESHDermatitis, Contact/pathology-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHEar-
dc.subject.MESHInterleukin-17/immunology*-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred BALB C-
dc.subject.MESHMicroscopy, Electron-
dc.subject.MESHReal-Time Polymerase Chain Reaction-
dc.subject.MESHTh2 Cells/metabolism-
dc.subject.MESHWater Loss, Insensible/physiology-
dc.titleThe role of interleukin-17 in mouse models of atopic dermatitis and contact dermatitis-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentYonsei Biomedical Research Center (연세의생명연구원)-
dc.contributor.googleauthorW. I. Heo-
dc.contributor.googleauthorK. E. Lee-
dc.contributor.googleauthorJ. Y. Hong-
dc.contributor.googleauthorM. N. Kim-
dc.contributor.googleauthorM. S. Oh-
dc.contributor.googleauthorY. S. Kim-
dc.contributor.googleauthorK. W. Kim-
dc.contributor.googleauthorK. E. Kim-
dc.contributor.googleauthorM. H. Sohn-
dc.identifier.doi10.1111/ced.12567-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01967-
dc.contributor.localIdA02363-
dc.contributor.localIdA04431-
dc.contributor.localIdA00303-
dc.contributor.localIdA00327-
dc.contributor.localIdA00441-
dc.contributor.localIdA00791-
dc.relation.journalcodeJ00549-
dc.identifier.pmid25684357-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1111/ced.12567/abstract-
dc.contributor.alternativeNameSon, Myung Hyun-
dc.contributor.alternativeNameOh, Mi Seon-
dc.contributor.alternativeNameHong, Jung Yeon-
dc.contributor.alternativeNameKim, Kyung Won-
dc.contributor.alternativeNameKim, Kyu Earn-
dc.contributor.alternativeNameKim, Mina-
dc.contributor.alternativeNameKim, Yun Seon-
dc.contributor.affiliatedAuthorSon, Myung Hyun-
dc.contributor.affiliatedAuthorOh, Mi Seon-
dc.contributor.affiliatedAuthorHong, Jung Yeon-
dc.contributor.affiliatedAuthorKim, Kyung Won-
dc.contributor.affiliatedAuthorKim, Kyu Earn-
dc.contributor.affiliatedAuthorKim, Mina-
dc.contributor.affiliatedAuthorKim, Yun Seon-
dc.rights.accessRightsnot free-
dc.citation.volume40-
dc.citation.number6-
dc.citation.startPage665-
dc.citation.endPage671-
dc.identifier.bibliographicCitationClinical and Experimental Dermatology, Vol.40(6) : 665-671, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아청소년과학교실) > 1. Journal Papers

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