{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T04:48:27Z","timestamp":1777610907750,"version":"3.51.4"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2021,11,3]],"date-time":"2021-11-03T00:00:00Z","timestamp":1635897600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","award":["JP26461465"],"award-info":[{"award-number":["JP26461465"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","award":["JP15H06454"],"award-info":[{"award-number":["JP15H06454"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","award":["JP16H06276"],"award-info":[{"award-number":["JP16H06276"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","award":["JP17K15665"],"award-info":[{"award-number":["JP17K15665"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001700","name":"Ministry of Education, Culture, Sports, Science and Technology","doi-asserted-by":"publisher","award":["JP19K07482"],"award-info":[{"award-number":["JP19K07482"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003837","name":"Ichiro Kanehara Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003837","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007449","name":"Takeda Science Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007449","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Nagao Memorial Fund"},{"name":"Kagawa University Young Scientists 2015"},{"name":"Kagawa University Research Promotion Program"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,2,23]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Type I IFNs (IFN-\u03b1 and IFN-\u03b2), immunomodulatory cytokines secreted from activated plasmacytoid dendritic cells (pDCs), contribute to the innate defense against pathogenic infections and the pathogenesis of the autoimmune disease psoriasis vulgaris. A previous study has shown that an E26 transformation-specific (Ets) family transcription factor Spi-B can transactivate the type I IFN promoter in synergy with IFN regulatory factor (IRF)-7 and is required for type I IFN production in pDCs. However, the mechanism of negative regulation of type I IFNs by pDCs remains unknown. In this study, we report that a basic leucine zipper (bZip) transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MafB) suppresses the induction of type I IFNs in pDCs. The elevated expression of MafB inhibited the transactivation of type I IFN genes in a dose-dependent manner. At the molecular level, MafB interacted with the Ets domain of Spi-B and interfered with IRF-7\u2013Spi-B complexation. Decreased MafB mRNA expression and degradation of MafB protein in the early phase of immune responses led to the enhancement of type I IFNs in pDCs. In vivo studies indicated that MafB is involved in resistance against imiquimod-induced psoriasis-like skin inflammation. Overall, these findings demonstrate that MafB acts as a negative regulator of type I IFN induction in pDCs and plays an important role in maintaining immune homeostasis.<\/jats:p>","DOI":"10.1093\/intimm\/dxab103","type":"journal-article","created":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T12:12:54Z","timestamp":1635768774000},"page":"159-172","source":"Crossref","is-referenced-by-count":13,"title":["Transcription factor MafB-mediated inhibition of type I interferons in plasmacytoid dendritic cells"],"prefix":"10.1093","volume":"34","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9189-4043","authenticated-orcid":false,"given":"Hiroyuki","family":"Saiga","sequence":"first","affiliation":[{"name":"Department of Immunology, Faculty of Medicine, Kagawa University , Miki, Kagawa , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaki","family":"Ueno","sequence":"additional","affiliation":[{"name":"Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University , Miki, Kagawa , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takashi","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Laboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical Science (IMS-RCAI) , Yokohama, Kanagawa , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tsuneyasu","family":"Kaisho","sequence":"additional","affiliation":[{"name":"Laboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical Science (IMS-RCAI) , Yokohama, Kanagawa , Japan"},{"name":"Department of Immunology, Institute of Advanced Medicine, Wakayama Medical University , Kimiidera, Wakayama , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0493-4815","authenticated-orcid":false,"given":"Katsuaki","family":"Hoshino","sequence":"additional","affiliation":[{"name":"Department of Immunology, Faculty of Medicine, Kagawa University , Miki, Kagawa , Japan"},{"name":"Laboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical Science (IMS-RCAI) , Yokohama, Kanagawa , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2021,11,3]]},"reference":[{"key":"2022063019204268900_CIT0001","doi-asserted-by":"crossref","first-page":"37","DOI":"10.1016\/j.immuni.2018.12.027","article-title":"Plasmacytoid dendritic cells: development, regulation, and function","volume":"50","author":"Reizis","year":"2019","journal-title":"Immunity"},{"key":"2022063019204268900_CIT0002","doi-asserted-by":"crossref","first-page":"305","DOI":"10.1016\/j.immuni.2010.03.012","article-title":"Intracellular toll-like receptors","volume":"32","author":"Blasius","year":"2010","journal-title":"Immunity"},{"key":"2022063019204268900_CIT0003","doi-asserted-by":"crossref","first-page":"949","DOI":"10.1038\/nature04641","article-title":"IkappaB kinase-alpha is critical for interferon-alpha production induced by Toll-like receptors 7 and 9","volume":"440","author":"Hoshino","year":"2006","journal-title":"Nature"},{"key":"2022063019204268900_CIT0004","doi-asserted-by":"crossref","first-page":"1061","DOI":"10.1038\/ni1118","article-title":"Interferon-alpha induction through Toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6","volume":"5","author":"Kawai","year":"2004","journal-title":"Nat. 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