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首页> 外文期刊>Journal of Molecular Biology >Caspase-1 Is an Apical Caspase Leading to Caspase-3 Cleavage in the AIM2 Inflammasome Response, Independent of Caspase-8
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Caspase-1 Is an Apical Caspase Leading to Caspase-3 Cleavage in the AIM2 Inflammasome Response, Independent of Caspase-8

机译：Caspase-1是Apical Caspase，其导致Aim2炎症组的Caspase-3切割，与Caspase-8无关

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Abstract Canonical inflammasomes are multiprotein complexes that can activate both caspase-1 and caspase-8. Caspase-1 drives rapid lysis of cells by pyroptosis and maturation of interleukin (IL)-1β and IL-18. In caspase-1-deficient cells, inflammasome formation still leads to caspase-3 activation and slower apoptotic death, dependent on caspase-8 as an apical caspase. A role for caspase-8 directly upstream of caspase-1 has also been suggested, but here we show that caspase-8-deficient macrophages have no defect in AIM2 inflammasome-mediated caspase-1 activation, pyroptosis, and IL-1β cleavage. In investigating the inflammasome-induced apoptotic pathway, we previously demonstrated that activated caspase-8 is essential for caspase-3 cleavage and apoptosis in caspase-1-deficient cells. However, here we found that AIM2 inflammasome-initiated caspase-3 cleavage was maintained in Ripk3 ?/? Casp8 ?/? macrophages. Gene knockdown showed that caspase-1 was required for the caspase-3 cleavage. Thus inflammasomes activate a network of caspases that can promote both pyroptotic and apoptotic cell death. In cells where rapid pyroptosis is blocked, delayed inflammasome-dependent cell death could still occur due to both caspase-1- and caspase-8-dependent apoptosis. Initiation of redundant cell death pathways is likely to be a strategy for coping with pathogen interference in death processes. Graphical Abstract Display Omitted Highlights ? Inflammasomes activate a network of caspases to initiate pyroptosis and apoptosis. ? Caspase-1 and caspase-8 are the inflammasome apical caspases. ? AIM2 inflammasome activates caspase-1 independent of caspase-8. ? Caspase-1 and caspase-8 are both upstream of caspase-3 cleavage initiated by AIM2. ? Redundant death pathways may combat pathogen evasion strategies.
机译：摘要规范炎症是多素蛋白复合物，其可以激活半胱天冬酶-1和Caspase-8。 Caspase-1通过糊酶和白细胞介素（IL）-1β和IL-18的成熟来驱动细胞的快速溶解。在Caspase-1缺乏细胞中，炎症组仍然导致Caspase-3活化和较慢的凋亡死亡，依赖于Caspase-8作为顶级胱天蛋白酶。还提出了Caspase-8直接上游的作用，但在这里，我们表明Caspase-8缺陷巨噬细胞在Aim2炎症介导的Caspase-1活化，糊酶和IL-1β切割中没有缺陷。在研究炎症诱导的凋亡途径时，我们之前证明了活化的Caspase-8对于Caspase-3裂解细胞中的Caspase-3切割和细胞凋亡至关重要。但是，在这里，我们发现Aim2发炎的Caspase-3裂解在RIPK3中保持？/？ Casp8？/？巨噬细胞。基因敲低显示Caspase-3裂解需要Caspase-1。因此，炎性炎症激活半胱天冬酶的网络，可以促进糊化和凋亡细胞死亡。在封闭快速胃癌的细胞中，由于Caspase-1-和Caspase-8依赖性凋亡，仍然可能发生延迟的炎症组细胞死亡。冗余细胞死亡途径的启动可能是应对死亡过程中病原体干扰的策略。图形抽象显示省略了亮点？炎症瘤激活半胱天冬酶的网络以引发糊化酶和细胞凋亡。还是Caspase-1和Caspase-8是炎症组顶型木蛋白酶。还是AIM2炎性炎症使Caspase-1独立于Caspase-8激活。还是Caspase-1和Caspase-8均在Aim2发起的Caspase-3裂解的上游。还是冗余死亡途径可以打击病原体逃避策略。

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