Possible roles of adiponetin in a mouse model of psoriasis

Research Project

Project/Area Number	25860935
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Dermatology
Research Institution	The University of Tokyo
Principal Investigator	SHIBATA Sayaka 東京大学, 医学部附属病院, 助教 (50613105)
Project Period (FY)	2013-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000) Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000) Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Keywords	乾癬 / アディポネクチン / イミキモド乾癬様皮膚炎モデル
Outline of Final Research Achievements	Accumulating epidemiologic evidence has revealed that metabolic syndrome is an independent risk factor for psoriasis development and is associated with more severe psoriasis. Adiponectin, primarily recognized as a metabolic mediator of insulin sensitivity, has been newly drawing attention as a mediator of immune responses. Here we demonstrate that adiponectin regulates skin inflammation, especially IL-17-related psoriasiform dermatitis. Mice with adiponectin deficiency show severe psoriasiform skin inflammation with enhanced infiltration of IL-17-producing dermal gd T cells. Adiponectin directly acts on murine dermal gd T cells to suppress IL-17 synthesis via AdipoR1. We furthermore demonstrate here that exogenous adiponectin rescues exacerbated dermatitis in adiponetin knock-out mice. Our data provide a regulatory role of adiponectin in skin inflammation, which would imply a mechanism underlying the relationship between psoriasis and metabolic disorders.