Inflammasomes are intracellular protein complexes consisting of the pattern recognition receptors and inflammatory molecules in the inflamed cells. In response to various ligands, inflammasomes play a pivotal role to execute the inflammatory responses by inducing the pyroptosis and the secretion of pro-inflammatory cytokines, interleukin (IL)-1β, and IL-18. Unlike canonical inflammasomes, including NOD-like receptor family inflammasomes, such as NLRP1, NLRP3, NLRC4, and absence in melanoma 2 inflammasomes, noncanonical inflammasomes, such as mouse caspase-11 and human caspase-4/5 were recently discovered, and their roles in the inflammatory responses have been poorly understood. However, emerging studies have been successfully demonstrating the regulatory roles of these noncanonical inflammasomes on inflammatory responses and the pathogenesis of inflammatory/autoimmune diseases. This review summarizes and discusses the recent studies investigating the regulatory roles of the caspase-11 noncanonical inflammasome in neuroinflammation and the pathogenesis of multiple sclerosis (MS), which provides the insight for the validation of caspase-11 noncanonical inflammasome to develop novel and promising therapeutics for MS.
Neuroimmunomodulation

中文翻译：

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Caspase-11 非经典炎症小体：神经炎症和多发性硬化症小鼠模型中的新关键参与者

炎症小体是由模式识别受体和炎症细胞中的炎症分子组成的细胞内蛋白质复合物。响应于各种配体，炎症小体通过诱导细胞焦亡和促炎细胞因子、白细胞介素 (IL)-1β 和 IL-18 的分泌，在执行炎症反应方面发挥着关键作用。与经典炎症小体不同，包括 NOD 样受体家族炎症小体，如 NLRP1、NLRP3、NLRC4 和黑色素瘤 2 炎症小体的缺失，最近发现了非经典炎症小体，如小鼠 caspase-11 和人 caspase-4/5，以及它们的作用对炎症反应知之甚少。然而，新兴研究已成功证明这些非经典炎症小体对炎症反应和炎症/自身免疫疾病的发病机制的调节作用。本综述总结并讨论了最近研究 caspase-11 非典型炎症小体在神经炎症和多发性硬化症 (MS) 发病机制中的调节作用的研究，为验证 caspase-11 非典型炎症小体以开发新的和有前景的治疗方法提供了见解形式。
神经免疫调节