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2014 Fiscal Year Final Research Report

Possible roles of adiponetin in a mouse model of psoriasis

Research Project

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Project/Area Number 25860935
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Dermatology
Research InstitutionThe 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
Keywords乾癬 / アディポネクチン
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.

Free Research Field

皮膚科学

URL: 

Published: 2016-06-03  

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