Mitochondrial Reactive Oxygen Species Are Essential for the Development of Psoriatic Inflammation
In: Frontiers in Immunology, Jg. 12 (2021-08-01)
Online
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Zugriff:
Psoriasis is a common immune-mediated, chronic, inflammatory skin disease that affects approximately 2–3% of the population worldwide. Although there is increasing evidence regarding the essential roles of the interleukin (IL)-23/IL-17 axis and dendritic cell (DC)-T cell crosstalk in the development of skin inflammation, the contributions of mitochondrial function to psoriasis are unclear. In a mouse model of imiquimod (IMQ)-induced psoriasiform skin inflammation, we found that hematopoietic cell-specific genetic deletion of p32/C1qbp, a regulator of mitochondrial protein synthesis and metabolism, protects mice from IMQ-induced psoriatic inflammation. Additionally, we demonstrate that p32/C1qbp is an important regulator of IMQ-induced DC activation, both in vivo and in vitro. We also found that p32/C1qbp-deficient DCs exhibited impaired production of IL-1β, IL-23, and mitochondrial reactive oxygen species (mtROS) after IMQ stimulation. Because the inhibition of mtROS suppressed IMQ-induced DC activation and psoriatic inflammation, we presume that p32/C1qbp and mtROS can serve as therapeutic targets in psoriasis.
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Mitochondrial Reactive Oxygen Species Are Essential for the Development of Psoriatic Inflammation
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Autor/in / Beteiligte Person: | Mizuguchi, Soichi ; Gotoh, Kazuhito ; Nakashima, Yuya ; Setoyama, Daiki ; Takata, Yurie ; Ohga, Shouichi ; Kang, Dongchon |
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Zeitschrift: | Frontiers in Immunology, Jg. 12 (2021-08-01) |
Veröffentlichung: | Frontiers Media S.A., 2021 |
Medientyp: | unknown |
ISSN: | 1664-3224 (print) |
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