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Interleukin-1 and tumor necrosis factor-α trigger restriction of hepatitis B virus infection via a cytidine deaminase activation-induced cytidine deaminase (AID).
https://doi.org/10.24517/00053812
https://doi.org/10.24517/00053812fe3e0adf-66f7-46f0-83ed-7f5c48dde677
| 名前 / ファイル | ライセンス | アクション |
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ME-PR-KITAMURA-K-31715-27.pdf (2.8 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2019-04-05 | |||||||||
| タイトル | ||||||||||
| タイトル | Interleukin-1 and tumor necrosis factor-α trigger restriction of hepatitis B virus infection via a cytidine deaminase activation-induced cytidine deaminase (AID). | |||||||||
| 言語 | ||||||||||
| 言語 | eng | |||||||||
| 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 | |||||||||
| ID登録 | ||||||||||
| ID登録 | 10.24517/00053812 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Watashi, Koichi
× Watashi, Koichi× Liang, Guoxin× Iwamoto, Masashi× Marusawa, Hiroyuki× Uchida, Nanako× Daito, Takuji× Kitamura, Kouichi× Muramatsu, Masamichi× Ohashi, Hirofumi× Kiyohara, Tomoko× Suzuki, Ryosuke× Li, Jisu× Tong, Shuping× Tanaka, Yasuhito× Murata, Kazumoto× Aizaki, Hideki× Wakita, Takaji |
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| 著者別表示 |
喜多村, 晃一
× 喜多村, 晃一
× 村松, 正道
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| 提供者所属 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 金沢大学医薬保健研究域医学系 | |||||||||
| 書誌情報 |
Journal of Biological Chemistry 巻 288, 号 44, p. 31715-31727, 発行日 2013-11-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 0021-9258 | |||||||||
| NCID | ||||||||||
| 収録物識別子タイプ | NCID | |||||||||
| 収録物識別子 | AA00251083 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isIdenticalTo | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.1074/jbc.M113.501122 | |||||||||
| 出版者 | ||||||||||
| 出版者 | American Society for Biochemistry and Molecular Biology Inc. | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Virus infection is restricted by intracellular immune responses in host cells, and this is typically modulated by stimulation of cytokines. The cytokines and host factors that determine the host cell restriction against hepatitis B virus (HBV) infection are not well understood. We screened 36 cytokines and chemokines to determine which were able to reduce the susceptibility of HepaRG cells to HBV infection. Here, we found that pretreatment with IL-1β and TNFα remarkably reduced the host cell susceptibility to HBV infection. This effect was mediated by activation of the NF-κB signaling pathway. A cytidine deaminase, activation-induced cytidine deaminase (AID), was up-regulated by both IL-1β and TNFα in a variety of hepatocyte cell lines and primary human hepatocytes. Another deaminase APOBEC3G was not induced by these proinflammatory cytokines. Knockdown of AID expression impaired the anti-HBV effect of IL-1β, and overexpression of AID antagonized HBV infection, suggesting that AID was one of the responsible factors for the anti-HBV activity of IL-1/TNFα. Although AID induced hypermutation of HBV DNA, this activity was dispensable for the anti-HBV activity. The antiviral effect of IL-1/TNFα was also observed on different HBV genotypes but not on hepatitis C virus. These results demonstrate that proinflammatory cytokines IL-1/TNFα trigger a novel antiviral mechanism involving AID to regulate host cell permissiveness to HBV infection. | |||||||||
| 権利 | ||||||||||
| 権利情報 | Copyright © 2013 by The American Society for Biochemistry and Molecular Biology, Inc. | |||||||||
| 著者版フラグ | ||||||||||
| 出版タイプ | VoR | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
| 関連URI | ||||||||||
| 識別子タイプ | URI | |||||||||
| 関連識別子 | http://www.jbc.org/content/288/44/31715 | |||||||||
| 関連名称 | http://www.jbc.org/content/288/44/31715 | |||||||||
