Lupfer Christopher, Malik Ankit, Kanneganti Thirumala-Devi
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, United States.
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, United States.
Curr Opin Virol. 2015 Jun;12:38-46. doi: 10.1016/j.coviro.2015.02.007. Epub 2015 Mar 12.
The inflammasome is a caspase-1 containing complex that activates the proinflammatory cytokines IL-1β and IL-18 and results in the proinflammatory cell death known as pyroptosis. Numerous recent publications have highlighted the importance of inflammasome activation in the control of virus infection. Inflammasome activation during viral infection is dependent on a variety of upstream receptors including the NOD-like receptor, RIG-I-like receptor and AIM2-like receptor families. Various receptors also function in inflammasome activation in different cellular compartments, including the cytoplasm and the nucleus. The effectiveness of inflammasomes at suppressing virus replication is highlighted by the prevalence and diversity of virus encoded inflammasome inhibitors. Also, the host has a myriad of regulatory mechanisms in place to prevent unwanted inflammasome activation and overt inflammation. Finally, recent reports begin to suggest that inflammasome activation and inflammasome modulation may have important clinical applications. Herein, we highlight recent advances and discuss potential future directions toward understanding the role of inflammasomes during virus infection.
炎性小体是一种含有半胱天冬酶-1的复合物,可激活促炎细胞因子IL-1β和IL-18,并导致称为细胞焦亡的促炎性细胞死亡。最近的大量出版物强调了炎性小体激活在控制病毒感染中的重要性。病毒感染期间炎性小体的激活依赖于多种上游受体,包括NOD样受体、RIG-I样受体和AIM2样受体家族。各种受体也在不同的细胞区室(包括细胞质和细胞核)的炎性小体激活中发挥作用。病毒编码的炎性小体抑制剂的普遍性和多样性突出了炎性小体在抑制病毒复制方面的有效性。此外,宿主有大量的调节机制来防止不必要的炎性小体激活和过度炎症。最后,最近的报告开始表明炎性小体激活和炎性小体调节可能具有重要的临床应用。在此,我们重点介绍最近的进展,并讨论在理解病毒感染期间炎性小体的作用方面潜在的未来方向。