泛素在天然抗病毒免疫的激活与衰减中的作用
Ubiquitin in the activation and attenuation of innate antiviral immunity.
作者信息
Heaton Steven M, Borg Natalie A, Dixit Vishva M
机构信息
Infection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia.
Infection and Immunity Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia
出版信息
J Exp Med. 2016 Jan 11;213(1):1-13. doi: 10.1084/jem.20151531. Epub 2015 Dec 28.
Viral infection activates danger signals that are transmitted via the retinoic acid-inducible gene 1-like receptor (RLR), nucleotide-binding oligomerization domain-like receptor (NLR), and Toll-like receptor (TLR) protein signaling cascades. This places host cells in an antiviral posture by up-regulating antiviral cytokines including type-I interferon (IFN-I). Ubiquitin modifications and cross-talk between proteins within these signaling cascades potentiate IFN-I expression, and inversely, a growing number of viruses are found to weaponize the ubiquitin modification system to suppress IFN-I. Here we review how host- and virus-directed ubiquitin modification of proteins in the RLR, NLR, and TLR antiviral signaling cascades modulate IFN-I expression.
病毒感染会激活危险信号，这些信号通过视黄酸诱导基因1样受体（RLR）、核苷酸结合寡聚化结构域样受体（NLR）和Toll样受体（TLR）蛋白信号级联进行传递。这通过上调包括I型干扰素（IFN-I）在内的抗病毒细胞因子，使宿主细胞处于抗病毒状态。这些信号级联中蛋白质之间的泛素修饰和相互作用增强了IFN-I的表达，相反，越来越多的病毒被发现利用泛素修饰系统来抑制IFN-I。在此，我们综述了RLR、NLR和TLR抗病毒信号级联中宿主和病毒导向的蛋白质泛素修饰如何调节IFN-I的表达。
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