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

Authors
 Joonsung Hwang  ;  Ryosuke Kita  ;  Hyouk-Soo Kwon  ;  Eung Ho Choi  ;  Seung Hun Lee  ;  Mark C. Udey  ;  Maria I. Morasso 
Citation
 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol.108(28) : 11566-11571, 2011 
Journal Title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN
 0027-8424 
Issue Date
2011
MeSH
Animals ; Cell Differentiation ; Cytokines/biosynthesis ; Dermatitis/etiology* ; Dermatitis/genetics ; Dermatitis/immunology ; Dermatitis/pathology ; Disease Models, Animal ; Epidermis/immunology ; Epidermis/pathology ; Female ; Homeodomain Proteins/genetics ; Homeodomain Proteins/immunology* ; Humans ; Hyperplasia ; Inflammation Mediators/metabolism ; Interleukin-17/metabolism* ; Keratinocytes/immunology ; Keratinocytes/pathology ; Leukocytes/immunology ; Leukocytes/pathology ; Mice ; Mice, Knockout ; Pregnancy ; Th17 Cells/immunology ; Th17 Cells/pathology ; Transcription Factors/deficiency* ; Transcription Factors/genetics ; Transcription Factors/immunology*
Abstract
In 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.
Files in This Item:
T201102003.pdf Download
DOI
10.1073/pnas.1019658108
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
Yonsei Authors
Lee, Seung Hun(이승헌)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/93434
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