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Blockade of the CXCR3/CXCL10 axis ameliorates inflammation caused by immunoproteasome dysfunction
| 名前 / ファイル | ライセンス | アクション |
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jci_7_7_e152681.pdf (6.21 MB)
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| Item type | 文献 / Documents(1) | |||||||||||||||||||||||||||||||||||
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| 公開日 | 2022-07-22 | |||||||||||||||||||||||||||||||||||
| アクセス権 | ||||||||||||||||||||||||||||||||||||
| アクセス権 | open access | |||||||||||||||||||||||||||||||||||
| 資源タイプ | ||||||||||||||||||||||||||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||||||||||||||||||||||||
| 資源タイプ | journal article | |||||||||||||||||||||||||||||||||||
| 出版社版DOI | ||||||||||||||||||||||||||||||||||||
| 関連識別子 | https://doi.org/10.1172/jci.insight.152681 | |||||||||||||||||||||||||||||||||||
| 関連名称 | 10.1172/jci.insight.152681 | |||||||||||||||||||||||||||||||||||
| 出版タイプ | ||||||||||||||||||||||||||||||||||||
| 出版タイプ | VoR | |||||||||||||||||||||||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||||||||||||||||||||||||||
| タイトル | ||||||||||||||||||||||||||||||||||||
| タイトル | Blockade of the CXCR3/CXCL10 axis ameliorates inflammation caused by immunoproteasome dysfunction | |||||||||||||||||||||||||||||||||||
| 著者 |
佐々木, 由紀
× 佐々木, 由紀× 有持, 秀喜
WEKO
1616
× 大塚, 邦紘
WEKO
954
× 近藤, 博之
WEKO
1192
× 九十九, 伸一
WEKO
1556
× 安友, 康二
WEKO
1521
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| 内容記述 | 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. | |||||||||||||||||||||||||||||||||||
| 書誌情報 |
en : JCI Insight 巻 7, 号 7, p. e152681, 発行日 2022-04-08 |
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| 収録物識別子タイプ | ISSN | |||||||||||||||||||||||||||||||||||
| 収録物識別子 | 23793708 | |||||||||||||||||||||||||||||||||||
| 出版者 | ||||||||||||||||||||||||||||||||||||
| 出版者 | American Society for Clinical Investigation | |||||||||||||||||||||||||||||||||||
| 権利情報 | ||||||||||||||||||||||||||||||||||||
| 権利情報 | This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/). | |||||||||||||||||||||||||||||||||||
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| 識別子 | 385113 | |||||||||||||||||||||||||||||||||||
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| 言語 | eng | |||||||||||||||||||||||||||||||||||
