期刊
NATURE IMMUNOLOGY
卷 14, 期 4, 页码 346-355出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2535
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资金
- Global Research Laboratory program of the Ministry of Education, Science and Technology of Korea (MEST) [K20704000006-10A0500-00610]
- World Class University program
- Korean government (MEST) through the National Research Foundation of Korea [R312010000100860]
- National Research Foundation of Korea
- Korean government (MEST) [2012028272]
- Korea Genetically Engineered Mouse Center Program of the National Research Foundation of the Korean government (MEST) [2011-0020603]
The production of type I interferon is essential for viral clearance but is kept under tight control to avoid unnecessary tissue damage from hyperinflammatory responses. Here we found that OASL1 inhibited translation of IRF7, the master transcription factor for type I interferon, and thus negatively regulated the robust production of type I interferon during viral infection. OASL1 inhibited the translation of IRF7 mRNA by binding to the 5' untranslated region (UTR) of IRF7 and possibly by inhibiting scanning of the 43S preinitiation complex along the message. Oasl1(-/-) mice were resistant to viral infection because of the greater abundance of type I interferon, which suggests that OASL1 could be a potential therapeutic target for boosting the production of type I interferon during viral infection.
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