國家衛生研究院 NHRI:Item 3990099045/10326

NHRI > National Institute of Environmental Health Sciences > Shau-Ku Huang > Periodical Articles > Item 3990099045/10326

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/10326

Title:	Role of IL-17F in the pathogenesis of psoriasis
Authors:	Nakajima, M;Kawaguchi, M;Watanabe, H;Morishima, Y;Huang, SK;Satoh, H;Hizawa, N
Contributors:	National Institute of Environmental Health Sciences
Abstract:	Psoriasis is a complex autoimmune inflammatory disease with a genetic basis. The increased expression of IL-17F gene and protein is observed in the lesional skins of psoriatic patients. We and other groups discovered human IL-17F gene that shows the highest homology with IL-17A. IL-17F induces various inflammatory molecules, such as IL-6 and IL-8. IL-17F is mainly derived from Th17, Tc17 and ILC3 cells, and induces CCL20 expression, resulting in the recruitment of additional IL-17F-producing cells to enhance skin inflammation via CCR6. The receptor for IL-17F is the heterodimeric complex of IL-17RA and IL-17RC, and several signaling pathways have been identified. Injection with IL-17F in mice revealed marked neutrophilia in dermis, and its infiltration was significantly inhibited by anti-IL-8 antibody. Sequence variants of the IL-17F gene are associated with response to treatments, and a variant (rs763780) of IL-17F encodes an antagonist for the wild-type IL-17F. Hence, IL-17F may play a pivotal role in the pathogenesis of psoriasis, and may provide a promising therapeutic target for development of novel strategies.
Date:	2016-08
Relation:	Current Immunology Reviews. 2016 Aug;12(2):112-117.
Link to:	http://dx.doi.org/10.2174/1573395513666161214121923
Cited Times(Scopus):	http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85011012898
Appears in Collections:	[Shau-Ku Huang] Periodical Articles

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