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; Shinichi Sato

doi:10.1038/ncomms8687

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, Shinichi Sato

Research output: Contribution to journal › Article › peer-review

121 Citations (Scopus)

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.

Original language	English
Article number	7687
Journal	Nature communications
Volume	6
DOIs	https://doi.org/10.1038/ncomms8687
Publication status	Published - 2015 Jul 15
Externally published	Yes

ASJC Scopus subject areas

Chemistry(all)
Biochemistry, Genetics and Molecular Biology(all)
Physics and Astronomy(all)

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@article{7c6c5213e986483ba191845dbf5568e8,

title = "Adiponectin regulates psoriasiform skin inflammation by suppressing IL-17 production from γδ-T cells",

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.",

author = "Sayaka Shibata and Yayoi Tada and Hau, {Carren Sy} and Aya Mitsui and Masahiro Kamata and Yoshihide Asano and Makoto Sugaya and Takafumi Kadono and Yosuke Masamoto and Mineo Kurokawa and Toshimasa Yamauchi and Naoto Kubota and Takashi Kadowaki and Shinichi Sato",

note = "Funding Information: We thank Y. Ito, A and T. Kaga for tissue processing and staining, and C. Ohwashi, T. Ikegami and N. Watanabe for technical assistance. This work was supported by a grant for Research on Intractable Diseases from the Ministry of Health, Labour and Welfare of Japan. Publisher Copyright: {\textcopyright} 2015 Macmillan Publishers Limited. All rights reserved.",

year = "2015",

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day = "15",

doi = "10.1038/ncomms8687",

language = "English",

volume = "6",

journal = "Nature Communications",

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AU - Shibata, Sayaka

AU - Tada, Yayoi

AU - Hau, Carren Sy

AU - Mitsui, Aya

AU - Kamata, Masahiro

AU - Asano, Yoshihide

AU - Sugaya, Makoto

AU - Kadono, Takafumi

AU - Masamoto, Yosuke

AU - Kurokawa, Mineo

AU - Yamauchi, Toshimasa

AU - Kubota, Naoto

AU - Kadowaki, Takashi

AU - Sato, Shinichi

N1 - Funding Information: We thank Y. Ito, A and T. Kaga for tissue processing and staining, and C. Ohwashi, T. Ikegami and N. Watanabe for technical assistance. This work was supported by a grant for Research on Intractable Diseases from the Ministry of Health, Labour and Welfare of Japan. Publisher Copyright: © 2015 Macmillan Publishers Limited. All rights reserved.

PY - 2015/7/15

Y1 - 2015/7/15

N2 - 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.

AB - 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.

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

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