The antidiabetic agent metformin inhibits IL-23 production in murine bone-marrow-derived dendritic cells

Tomoyo Matsuda-Taniguchi, Masaki Takemura, Takeshi Nakahara, Akiko Hashimoto-Hachiya, Ayako Takai-Yumine, Masutaka Furue, Gaku Tsuji

研究成果: ジャーナルへの寄稿学術誌査読

1 被引用数 (Scopus)

抄録

Psoriasis is a chronic inflammatory skin disease, and its immune mechanism has been profoundly elucidated. Biologics targeting interleukin (IL)-23 have prevented the development of psoriasis. As major sources of IL-23, dendritic cells (DCs) play a pivotal role in psoriasis; however, the regulatory mechanism of IL-23 in DCs remains unclear. IL-36γ was reported to reflect the disease activity of psoriasis. Therefore, we hypothesized that IL-36γ may affect IL-23 production in DCs. To reveal the mechanism by which IL-36γ controls IL-23 production in DCs, we analyzed murine bone marrow-derived DCs (BMDCs) stimulated with IL-36γ. IL-36γ stimulation upregulated the mRNA and protein expression of Nfkbiz in BMDCs. Nfkbiz knockdown using siRNA transfection partially inhibited the upregulation of IL-23 mRNA expression induced by IL-36γ stimulation. Since NF-κB signaling regulates Nfkbiz expression and the anti-diabetic agent metformin reportedly modulates NF-κB signaling, we examined the effect of metformin treatment on IL-36γ-induced IL-23 production. Metformin treatment impaired the phosphorylation of NF-κB induced by IL-36γ stimulation with the subsequent downregulation of Nfkbiz, resulting in the inhibition of IL-23 production in BMDCs. These data provided evidence that metformin treatment can inhibit IL-36γ-mediated IL-23 production in BMDCs, which might contribute to the prevention of psoriasis.

本文言語英語
論文番号5610
ジャーナルJournal of Clinical Medicine
10
23
DOI
出版ステータス出版済み - 12月 1 2021

!!!All Science Journal Classification (ASJC) codes

  • 医学一般

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