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- W4366181684 abstract "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 using qRT-PCR, western blotting, and ELISA. 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 metformin, an antidiabetic agent, 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 suggest that metformin treatment can inhibit IL-36γ-mediated IL-23 production in BMDCs, which might be potentially effective in treating psoriasis in addition to diabetes mellitus." @default.
- W4366181684 created "2023-04-19" @default.
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- W4366181684 date "2023-05-01" @default.
- W4366181684 modified "2023-09-28" @default.
- W4366181684 title "023 The antidiabetic agent metformin inhibits IL-23 production in murine bone-marrow-derived dendritic cells" @default.
- W4366181684 doi "https://doi.org/10.1016/j.jid.2023.03.024" @default.
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