| First Author | Mizuguchi S | Year | 2021 |
| Journal | Front Immunol | Volume | 12 |
| Pages | 714897 | PubMed ID | 34421919 |
| Mgi Jnum | J:335340 | Mgi Id | MGI:6762251 |
| Doi | 10.3389/fimmu.2021.714897 | Citation | Mizuguchi S, et al. (2021) Mitochondrial Reactive Oxygen Species Are Essential for the Development of Psoriatic Inflammation. Front Immunol 12:714897 |
| abstractText | 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-1beta, 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. |
