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

Author

Listed:
  • Sayaka Shibata

    (University of Tokyo Graduate School of Medicine)

  • Yayoi Tada

    (University of Tokyo Graduate School of Medicine
    Teikyo Universtiy 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)

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.

Suggested Citation

  • 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 & , 2015. "Adiponectin regulates psoriasiform skin inflammation by suppressing IL-17 production from γδ-T cells," Nature Communications, Nature, vol. 6(1), pages 1-14, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8687
    DOI: 10.1038/ncomms8687
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