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Epidermal ablation of Dlx3 is linked to IL-17-associated skin inflammation

DC Field Value Language
dc.contributor.author이승헌-
dc.date.accessioned2014-12-20T16:49:03Z-
dc.date.available2014-12-20T16:49:03Z-
dc.date.issued2011-
dc.identifier.issn0027-8424-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/93434-
dc.description.abstractIn an effort to understand the role of Distal-less 3 (Dlx3) in cutaneous biology and pathophysiology, we generated and characterized a mouse model with epidermal ablation of Dlx3. K14cre;Dlx3(Kin/f) mice exhibited epidermal hyperproliferation and abnormal differentiation of keratinocytes. Results from subsequent analyses revealed cutaneous inflammation that featured accumulation of IL-17-producing CD4(+) T, CD8(+) T, and γδ T cells in the skin and lymph nodes of K14cre;Dlx3(Kin/f) mice. The gene expression signature of K14cre;Dlx3(Kin/f) skin shared features with lesional psoriatic skin, and Dlx3 expression was markedly and selectively decreased in psoriatic skin. Interestingly, cultured Dlx3 null keratinocytes triggered cytokine production that is potentially linked to inflammatory responses in K14cre;Dlx3(Kin/f) mice. Thus, Dlx3 ablation in epidermis is linked to altered epidermal differentiation, barrier development, and IL-17-associated skin inflammation. This model provides a platform that will allow the systematic exploration of the contributions of keratinocytes to cutaneous inflammation.-
dc.description.statementOfResponsibilityopen-
dc.format.extent11566~11571-
dc.relation.isPartOfPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-
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.MESHCell Differentiation-
dc.subject.MESHCytokines/biosynthesis-
dc.subject.MESHDermatitis/etiology*-
dc.subject.MESHDermatitis/genetics-
dc.subject.MESHDermatitis/immunology-
dc.subject.MESHDermatitis/pathology-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHEpidermis/immunology-
dc.subject.MESHEpidermis/pathology-
dc.subject.MESHFemale-
dc.subject.MESHHomeodomain Proteins/genetics-
dc.subject.MESHHomeodomain Proteins/immunology*-
dc.subject.MESHHumans-
dc.subject.MESHHyperplasia-
dc.subject.MESHInflammation Mediators/metabolism-
dc.subject.MESHInterleukin-17/metabolism*-
dc.subject.MESHKeratinocytes/immunology-
dc.subject.MESHKeratinocytes/pathology-
dc.subject.MESHLeukocytes/immunology-
dc.subject.MESHLeukocytes/pathology-
dc.subject.MESHMice-
dc.subject.MESHMice, Knockout-
dc.subject.MESHPregnancy-
dc.subject.MESHTh17 Cells/immunology-
dc.subject.MESHTh17 Cells/pathology-
dc.subject.MESHTranscription Factors/deficiency*-
dc.subject.MESHTranscription Factors/genetics-
dc.subject.MESHTranscription Factors/immunology*-
dc.titleEpidermal ablation of Dlx3 is linked to IL-17-associated skin inflammation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Dermatology (피부과학)-
dc.contributor.googleauthorJoonsung Hwang-
dc.contributor.googleauthorRyosuke Kita-
dc.contributor.googleauthorHyouk-Soo Kwon-
dc.contributor.googleauthorEung Ho Choi-
dc.contributor.googleauthorSeung Hun Lee-
dc.contributor.googleauthorMark C. Udey-
dc.contributor.googleauthorMaria I. Morasso-
dc.identifier.doi10.1073/pnas.1019658108-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02931-
dc.relation.journalcodeJ02550-
dc.identifier.eissn1091-6490-
dc.identifier.pmid21709238-
dc.contributor.alternativeNameLee, Seung Hun-
dc.contributor.affiliatedAuthorLee, Seung Hun-
dc.rights.accessRightsfree-
dc.citation.volume108-
dc.citation.number28-
dc.citation.startPage11566-
dc.citation.endPage11571-
dc.identifier.bibliographicCitationPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol.108(28) : 11566-11571, 2011-
dc.identifier.rimsid28231-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers

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