Interaction between Hepatitis B Virus and Toll-Like Receptors: Current Status and Potential Therapeutic Use for Chronic Hepatitis B.
Interaction between Hepatitis B Virus and Toll-Like Receptors: Current Status and Potential Therapeutic Use for Chronic Hepatitis B.
复制标题
DOI：
10.3390/vaccines6010006
复制
发表时间：
2018-01-16
期刊：
影响因子：
7.8
通讯作者：
Lu M
中科院分区：
文献类型：
--
作者：
Ma Z;Cao Q;Xiong Y;Zhang E;Lu M
针对B型肝炎病毒（HBV）感染的免疫防御是复杂的，涉及宿主的先天性和适应性免疫系统。众所周知，控制HBV感染需要发展足够的HBV特异性T细胞和B细胞应答。然而，近年来已经探索了先天免疫对清除HBV的贡献。Toll样受体（TLR）被认为是抗病毒免疫的第一线，因为它们启动细胞内信号传导途径以诱导抗病毒介质，如干扰素（IFN）和其他细胞因子。最近的研究表明，TLR介导的信号通路的激活导致体外和体内HBV复制的抑制。然而，HBV也发展了对抗TLR应答的策略，包括抑制TLR表达和阻断下游信号传导途径。慢性HBV感染患者的抗病毒治疗导致TLR表达上调并恢复其固有的抗病毒功能。因此，TLR激活可能作为一种额外的免疫选择，用于治疗慢性HBV感染与抗病毒治疗相结合。
Immune defense against infection with the hepatitis B virus (HBV) is complex and involves both host innate and adaptive immune systems. It is well accepted that the development of sufficient HBV-specific T cell and B cell responses are required for controlling an HBV infection. However, the contribution of innate immunity to removing HBV has been explored in recent years. Toll-like receptors (TLRs) are recognized as the first line of antiviral immunity because they initiate intracellular signaling pathways to induce antiviral mediators such as interferons (IFNs) and other cytokines. Recent studies show that the activation of TLR-mediated signaling pathways results in a suppression of HBV replication in vitro and in vivo. However, HBV has also evolved strategies to counter TLR responses including the suppression of TLR expression and the blockage of downstream signaling pathways. Antiviral treatment in chronic HBV-infected patients leads to an upregulation of TLR expression and the restoration of its innate antiviral functions. Thus, TLR activation may serve as an additional immunotherapeutic option for treating chronic HBV infection in combination with antiviral treatment.
登录
查看更多内容
影响因子：
13.5
作者：
Breiner, KM;Schaller, H;Knolle, PA
通讯作者：
Knolle, PA
DOI：
10.1016/j.clinre.2016.12.006
发表时间：
2017-09-01
影响因子：
2.7
作者：
Deng, Guangying;Ge, Jun;Zhang, Xiaoyong
通讯作者：
Zhang, Xiaoyong
影响因子：
5.5
作者：
Halperin, Scott A.;Ward, Brian;Martin, J. Tyler
通讯作者：
Martin, J. Tyler
影响因子：
6.2
作者：
Cooper, Curtis;Mackie, David
通讯作者：
Mackie, David
影响因子：
11.8
作者：
Cooper, C. L.;Angel, J. B.;Cameron, D. W.
通讯作者：
Cameron, D. W.