ZBP1 has been characterized as a critical innate immune sensor of not only viral RNA products but also endogenous nucleic acid ligands. ZBP1 sensing of the Z‐RNA produced during influenza virus infection induces cell death in the form of pyroptosis, apoptosis, and necroptosis (PANoptosis). PANoptosis is a coordinated cell death pathway that is driven through a multiprotein complex called the PANoptosome and enables crosstalk and co‐regulation among these processes. During influenza virus infection, a key step in PANoptosis and PANoptosome assembly is the formation of the ZBP1‐NLRP3 inflammasome. When Z‐RNA is sensed, ZBP1 recruits RIPK3 and caspase‐8 to activate the ZBP1‐NLRP3 inflammasome. Several other host factors have been found to be important for ZBP1‐NLRP3 inflammasome assembly, including molecules involved in the type I interferon signaling pathway and caspase‐6. Additionally, influenza viral proteins, such as M2, NS1, and PB1‐F2, have also been shown to regulate the ZBP1‐NLRP3 inflammasome. This review explains the functions of ZBP1 and the mechanistic details underlying the activation of the ZBP1‐NLRP3 inflammasome and the formation of the PANoptosome. Improved understanding of the ZBP1‐NLRP3 inflammasome will direct the development of therapeutic strategies to target infectious and inflammatory diseases.

中文翻译：

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ZBP1-NLRP3 炎症小体的调节及其在细胞焦亡、细胞凋亡和坏死性凋亡 (PANoptosis) 中的影响。

ZBP1 已被表征为不仅是病毒 RNA 产物而且也是内源性核酸配体的关键先天免疫传感器。ZBP1 感应流感病毒感染期间产生的 Z-RNA，以细胞焦亡、细胞凋亡和坏死性凋亡 (PANoptosis) 的形式诱导细胞死亡。PANoptosis 是一种协调的细胞死亡途径，它通过称为 PANoptosome 的多蛋白复合物驱动，并能够在这些过程之间进行串扰和协同调节。在流感病毒感染期间，PANoptosis 和 PANoptosis 组装的关键步骤是 ZBP1-NLRP3 炎性体的形成。当检测到 Z-RNA 时，ZBP1 会招募 RIPK3 和 caspase-8 来激活 ZBP1-NLRP3 炎症小体。已经发现其他几个宿主因素对 ZBP1-NLRP3 炎性体组装很重要，包括参与 I 型干扰素信号通路和 caspase-6 的分子。此外，流感病毒蛋白，如 M2、NS1 和 PB1-F2，也已被证明可以调节 ZBP1-NLRP3 炎症小体。本综述解释了 ZBP1 的功能以及 ZBP1-NLRP3 炎症小体激活和 PANoptosome 形成的机制细节。对 ZBP1-NLRP3 炎症小体的深入了解将指导针对传染性和炎症性疾病的治疗策略的开发。