Document Detail


Up-regulation of interleukin-13 receptor alpha1 on human keratinocytes in the skin of psoriasis and atopic dermatitis.
MedLine Citation:
PMID:  14527737     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Interleukin (IL)-13 is a pleiotropic cytokine, which shares many biological functions with IL-4. The receptor subunits of IL-13 consist of IL-4Ralpha, IL-13Ralpha1 and IL-13Ralpha2. The regulatory mechanisms of the IL-13Ralpha expression in the keratinocytes of certain skin disease have not been known. OBJECTIVE: To clear the roles of IL-13 and the regulatory mechanisms of its receptor in atopic dermatitis (AD) and psoriasis. METHOD: The expression of IL-13Ralpha1 in the skin of AD and psoriasis was investigated by immunohistochemistry. The regulation of IL-13Ralpha mRNA in the skin and human primary keratinocyte (HPK) was investigated by quantitative PCR. The secretion of IL-6 and RANTES from HPK was measured by ELISA. RESULTS: The expression of IL-13Ralpha1 was more prominent on the suprabasal keratinocytes in the skin of AD and striking increase of staining was observed on all layers of keratinocyte in the skin of psoriasis. The mRNA of IL-13Ralpha1, but not of IL-13Ralpha2 was overexpressed in both skin of AD and psoriasis. In vitro experiment using HPK demonstrated that IFN-gamma, IL-13 but not IL-4 could up-regulate the mRNA expression of IL-13Ralpha1. In contrast, IL-13Ralpha2 mRNA expression was up-regulated by IFN-gamma plus IL-4. Furthermore, the stimulation of HPK with IFN-gamma plus IL-13 and/or IL-4 resulted in significant enhancement of IL-6 and RANTES secretion. CONCLUSION: These findings indicate that IL-4 and IL-13 have different regulatory effects on the expression of IL-13Ralpha1 and alpha2, and the overexpression of IL-13Ralpha1 may play some roles in the pathogenesis of chronic stage of AD or psoriasis.
Authors:
Jongkonnee Wongpiyabovorn; Hajime Suto; Hiroko Ushio; Kenji Izuhara; Koichi Mitsuishi; Shigaku Ikeda; Atsuhito Nakao; Ko Okumura; Hideoki Ogawa
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of dermatological science     Volume:  33     ISSN:  0923-1811     ISO Abbreviation:  J. Dermatol. Sci.     Publication Date:  2003 Oct 
Date Detail:
Created Date:  2003-10-06     Completed Date:  2004-05-25     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9011485     Medline TA:  J Dermatol Sci     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  31-40     Citation Subset:  IM    
Affiliation:
Department of Dermatology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
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MeSH Terms
Descriptor/Qualifier:
Cells, Cultured
Cytokines / metabolism
Dermatitis, Atopic / metabolism*
Humans
Immunohistochemistry
Inflammation Mediators / metabolism
Interferon-gamma / pharmacology
Interleukin-13 / pharmacology
Interleukin-13 Receptor alpha1 Subunit
Interleukin-4 / pharmacology
Keratinocytes / drug effects,  metabolism*
Protein Isoforms / genetics,  metabolism
Psoriasis / metabolism*
RNA, Messenger / metabolism
Receptors, Interleukin / genetics,  metabolism*
Receptors, Interleukin-13
Skin / metabolism
Up-Regulation
Chemical
Reg. No./Substance:
0/Cytokines; 0/IL13RA1 protein, human; 0/Inflammation Mediators; 0/Interleukin-13; 0/Interleukin-13 Receptor alpha1 Subunit; 0/Protein Isoforms; 0/RNA, Messenger; 0/Receptors, Interleukin; 0/Receptors, Interleukin-13; 207137-56-2/Interleukin-4; 82115-62-6/Interferon-gamma

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