Cell Biology Unit, IRCCS AOU San Martino, IST Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy.
J Leukoc Biol. 2012 Nov;92(5):951-8. doi: 10.1189/jlb.0512265. Epub 2012 Aug 2.
Shifts in the redox balance between ROS and antioxidants regulate innate immunity at various levels. Changes in the redox microenvironment modulate the activation potential of the NLRP3 inflammasome, a signaling platform that activates caspase-1, allowing the maturation of IL-1β. However, a clear definition of the underlying mechanism is missing. In this essay, I review the most-credited theories on inflammasome activation. In particular, I will focus on the redox-mediated mechanisms that regulate the assembly of NLRP3 inflammasome and discuss how aberrations in them are implicated in the pathogenesis of autoinflammatory diseases.
ROS 和抗氧化剂之间的氧化还原平衡的变化在多个层面上调节先天免疫。氧化还原微环境的变化调节 NLRP3 炎性体的激活潜能,NLRP3 炎性体是一种激活 caspase-1 的信号平台,允许 IL-1β 的成熟。然而,潜在机制尚不清楚。在这篇文章中,我回顾了关于炎性体激活的最可信的理论。特别是,我将重点介绍调节 NLRP3 炎性体组装的氧化还原介导机制,并讨论它们的异常如何与自身炎症性疾病的发病机制有关。