| ○種別 (必須): | □ | 学術論文 (審査論文)
| [継承] |
| ○言語 (必須): | □ | 英語
| [継承] |
| ○招待 (推奨): |
| ○審査 (推奨): |
| ○カテゴリ (推奨): |
| ○共著種別 (推奨): |
| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | 佐々木 由紀 ([徳島大学.AWAサポートセンター])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 2. | 有持 秀喜 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.生体防御医学])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 3. | 大塚 邦紘 ([徳島大学.病院.先端歯科医療開発研究プロジェクト]/[徳島大学.病院.診療科.歯科口腔外科.口腔外科])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 4. | 近藤 博之 ([徳島大学.大学院医歯薬学研究部.医学域.先端医学教育研究プロジェクト]/[徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.生体防御医学])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 5. | 九十九 伸一 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.生体防御医学])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 6. | 安友 康二 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.生体防御医学])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| ○題名 (必須): | □ | (英) Blockade of the CXCR3/CXCL10 axis ameliorates inflammation caused by immunoproteasome dysfunction. (日)
| [継承] |
| ○副題 (任意): |
| ○要約 (任意): | □ | (英) Immunoproteasomes regulate the degradation of ubiquitin-coupled proteins and generate peptides that are preferentially presented by MHC class I. Mutations in immunoproteasome subunits lead to immunoproteasome dysfunction, which causes proteasome-associated autoinflammatory syndromes (PRAAS) characterized by nodular erythema and partial lipodystrophy. It remains unclear, however, how immunoproteasome dysfunction leads to inflammatory symptoms. Here, we established mice harboring a mutation in Psmb8 (Psmb8-KI mice) and addressed this question. Psmb8-KI mice showed higher susceptibility to imiquimod-induced skin inflammation (IMS). Blockade of IL-6 or TNF-α partially suppressed IMS in both control and Psmb8-KI mice, but there was still more residual inflammation in the Psmb8-KI mice than in the control mice. DNA microarray analysis showed that treatment of J774 cells with proteasome inhibitors increased the expression of the Cxcl9 and Cxcl10 genes. Deficiency in Cxcr3, the gene encoding the receptor of CXCL9 and CXCL10, in control mice did not change IMS susceptibility, while deficiency in Cxcr3 in Psmb8-KI mice ameliorated IMS. Taken together, these findings demonstrate that this mutation in Psmb8 leads to hyperactivation of the CXCR3 pathway, which is responsible for the increased susceptibility of Psmb8-KI mice to IMS. These data suggest the CXCR3/CXCL10 axis as a new molecular target for treating PRAAS. (日)
| [継承] |
| ○キーワード (推奨): |
| ○発行所 (推奨): |
| ○誌名 (必須): | □ | JCI Insight (American Society for Clinical Investigation)
(eISSN: 2379-3708)
| ○ISSN (任意): | □ | 2379-3708
ISSN: 2379-3708
(eISSN: 2379-3708) Title: JCI insightTitle(ISO): JCI InsightPublisher: American Society for Clinical Investigation (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
| [継承] |
| ○巻 (必須): | □ | 7
| [継承] |
| ○号 (必須): | □ | 7
| [継承] |
| ○頁 (必須): | □ |
| [継承] |
| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2022年 4月 8日 (令和 4年 4月 8日)
| [継承] |
| ○URL (任意): |
| ○DOI (任意): | □ | 10.1172/jci.insight.152681 (→Scopusで検索)
| [継承] |
| ○PMID (任意): | □ | 35393946 (→Scopusで検索)
| [継承] |
| ○CRID (任意): |
| ○WOS (任意): |
| ○Scopus (任意): |
| ○評価値 (任意): |
| ○被引用数 (任意): |
| ○指導教員 (推奨): |
| ○備考 (任意): | 1. | (英) PublicationType: Journal Article (日)
| [継承] |