Adiponectin regulates psoriasiform skin inflammation by suppressing IL-17 production from γδ-T cells

Sayaka Shibata, Yayoi Tada (), Carren Sy Hau, Aya Mitsui, Masahiro Kamata, Yoshihide Asano, Makoto Sugaya, Takafumi Kadono, Yosuke Masamoto, Mineo Kurokawa, Toshimasa Yamauchi, Naoto Kubota, Takashi Kadowaki and Shinichi Sato
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Sayaka Shibata: University of Tokyo Graduate School of Medicine
Yayoi Tada: University of Tokyo Graduate School of Medicine
Carren Sy Hau: Teikyo Universtiy School of Medicine
Aya Mitsui: University of Tokyo Graduate School of Medicine
Masahiro Kamata: University of Tokyo Graduate School of Medicine
Yoshihide Asano: University of Tokyo Graduate School of Medicine
Makoto Sugaya: University of Tokyo Graduate School of Medicine
Takafumi Kadono: University of Tokyo Graduate School of Medicine
Yosuke Masamoto: University of Tokyo Graduate School of Medicine
Mineo Kurokawa: University of Tokyo Graduate School of Medicine
Toshimasa Yamauchi: University of Tokyo Graduate School of Medicine
Naoto Kubota: University of Tokyo Graduate School of Medicine
Takashi Kadowaki: University of Tokyo Graduate School of Medicine
Shinichi Sato: University of Tokyo Graduate School of Medicine

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: Abstract 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 Vγ4+γδ-T cells. Adiponectin directly acts on murine dermal γδ-T cells to suppress IL-17 synthesis via AdipoR1. We furthermore demonstrate here that the adiponectin level of skin tissue as well as subcutaneous fat is decreased in psoriasis patients. IL-17 production from human CD4- or CD8-positive T cells is also suppressed by adiponectin. Our data provide a regulatory role of adiponectin in skin inflammation, which would imply a mechanism underlying the relationship between psoriasis and metabolic disorders.

Date: 2015
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DOI: 10.1038/ncomms8687

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