{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T00:31:45Z","timestamp":1792801905006,"version":"4.5.0"},"reference-count":71,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,8,6]],"date-time":"2021-08-06T00:00:00Z","timestamp":1628208000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Psoriasis is a common immune-mediated, chronic, inflammatory skin disease that affects approximately 2\u20133% 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 <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic>. We also found that p32\/C1qbp-deficient DCs exhibited impaired production of IL-1\u03b2, 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.<\/jats:p>","DOI":"10.3389\/fimmu.2021.714897","type":"journal-article","created":{"date-parts":[[2021,8,6]],"date-time":"2021-08-06T06:54:03Z","timestamp":1628232843000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":66,"title":["Mitochondrial Reactive Oxygen Species Are Essential for the Development of Psoriatic Inflammation"],"prefix":"10.3389","volume":"12","author":[{"given":"Soichi","family":"Mizuguchi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuhito","family":"Gotoh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuya","family":"Nakashima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daiki","family":"Setoyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yurie","family":"Takata","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shouichi","family":"Ohga","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongchon","family":"Kang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,8,6]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2230.2001.00832.x","article-title":"Psoriasis\u2013Epidemiology and Clinical Spectrum","volume":"26","author":"Christophers","year":"2001","journal-title":"Clin Exp Dermatol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/bjd.12230","article-title":"Is the Prevalence of Psoriasis Increasing? 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