期刊
JOURNAL OF INNATE IMMUNITY
卷 7, 期 1, 页码 47-58出版社
KARGER
DOI: 10.1159/000365113
关键词
Type I interferon; Hepatitis B virus regulation; Toll/IL-1R homology domain-containing adaptor molecule 1; Mitochondrial antiviral signaling protein; Pathogen-associated molecular patterns
类别
资金
- Ministry of Education, Science, and Culture
- Ministry of Health, Labor, and Welfare of Japan
- Yasuda Cancer Foundation
- Ono Foundation
- MEXT
- National Cancer Center Research and Development Fund [23-A-44]
- Japan Initiative for Global Research Network on Infectious Diseases (J-GRID)
- Grants-in-Aid for Scientific Research [26860593, 13J40020, 24590570] Funding Source: KAKEN
Toll-like receptors (TLRs) and cytoplasmic RNA sensors have been reported to be involved in the regulation of hepatitis B virus (HBV) replication, but remain controversial due to the lack of a natural infectious model. Our current study sets out to characterize aspects of the role of the innate immune system in eliminating HBV using hydrodynamic-based injection of HBV replicative plasmid and knockout mice deficient in specific pathways of the innate system. The evidence indicated that viral replication was not affected by MAVS or TICAM-1 knockout, but absence of interferon regulatory factor 3 (IRF-3) and IRF-7 transcription factors, as well as the interferon (IFN) receptor, had an adverse effect on the inhibition of HBV replication, demonstrating the dispensability of MAVS and TICAM-1 pathways in the early innate response against HBV. Myd88(-/-) mice did not have a significant increase in the initial viremia, but substantial viral antigen persisted in the mice sera, a response similar to Rag2(-/-) mice, suggesting that the MyD88-dependent pathway participated in evoking an adaptive immune response against the clearance of intrahepatic HBV. Taken together, we show that the RNA-sensing pathways do not participate in the regulation of HBV replication in a mouse model; meanwhile MyD88 is implicated in the HBV clearance. (C) 2014 S. Karger AG, Basel
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据