Okamoto Masaaki, Tsukamoto Hirotake, Kouwaki Takahisa, Seya Tsukasa, Oshiumi Hiroyuki
1 Department of Immunology, Faculty of Life Sciences, Graduate School of Medical Sciences, Kumamoto University , Kumamoto, Japan .
2 Department of Microbiology and Immunology, Graduate School of Medicine, Hokkaido University , Sapporo, Japan .
Viral Immunol. 2017 Jul/Aug;30(6):408-420. doi: 10.1089/vim.2016.0178. Epub 2017 Jun 13.
The innate immune system is the first line of defense against virus infection that triggers the expression of type I interferon (IFN) and proinflammatory cytokines. Pattern recognition receptors (PRRs) recognize pathogen-associated molecular patterns, resulting in the induction of innate immune responses. Viral RNA in endosomes is recognized by Toll-like receptors, and cytoplasmic viral RNA is recognized by RIG-I-like receptors. The host innate immune response is critical for protection against virus infection. However, it has been postulated that an excessive inflammatory response in the lung caused by the innate immune response is harmful to the host and is a cause of lethality during influenza A virus infection. Although the deletion of genes encoding PRRs or proinflammatory cytokines does not improve the mortality of mice infected with influenza A virus, a partial block of the innate immune response is successful in decreasing the mortality rate of mice without a loss of protection against virus infection. In addition, morbidity and mortality rates are influenced by other factors. For example, secondary bacterial infection increases the mortality rate in patients with influenza A virus and in animal models of the disease, and environmental factors, such as cigarette smoke and fine particles, also affect the innate immune response. In this review, we summarize recent findings related to the role of PRRs in innate immune response during respiratory viral infection.
先天免疫系统是抵御病毒感染的第一道防线,可触发I型干扰素(IFN)和促炎细胞因子的表达。模式识别受体(PRR)识别病原体相关分子模式,从而诱导先天免疫反应。内体中的病毒RNA由Toll样受体识别,细胞质中的病毒RNA由RIG-I样受体识别。宿主的先天免疫反应对于抵抗病毒感染至关重要。然而,据推测,先天免疫反应在肺部引起的过度炎症反应对宿主有害,是甲型流感病毒感染期间致死的一个原因。虽然缺失编码PRR或促炎细胞因子的基因并不能提高感染甲型流感病毒小鼠的存活率,但部分阻断先天免疫反应成功降低了小鼠的死亡率,同时又不丧失对病毒感染的保护作用。此外,发病率和死亡率还受其他因素影响。例如,继发细菌感染会增加甲型流感病毒患者及该疾病动物模型的死亡率,环境因素,如香烟烟雾和细颗粒物,也会影响先天免疫反应。在本综述中,我们总结了PRR在呼吸道病毒感染期间先天免疫反应中作用的最新研究结果。