裂谷1
程序性细胞死亡
细胞生物学
耶尔森尼亚
炎症反应
炎症
化学
生物
坏死性下垂
免疫学
细胞凋亡
遗传学
细菌
生物化学
作者
R.K. Subbarao Malireddi,Sannula Kesavardhana,Rajendra Karki,Balabhaskararao Kancharana,Amanda R. Burton,Thirumala‐Devi Kanneganti
出处
期刊:ImmunoHorizons
[The American Association of Immunologists]
日期:2020-12-01
卷期号:4 (12): 789-796
被引量:60
标识
DOI:10.4049/immunohorizons.2000097
摘要
Abstract Bacterial pathogens from the genus Yersinia cause fatal sepsis and gastritis in humans. Innate immune signaling and inflammatory cell death (pyroptosis, apoptosis, and necroptosis [PANoptosis]) serve as a first line of antimicrobial host defense. The receptor-interacting protein kinase 1 (RIPK1) is essential for Yersinia-induced pyroptosis and apoptosis and an effective host response. However, it is not clear whether RIPK1 assembles a multifaceted cell death complex capable of regulating caspase-dependent pyroptosis and apoptosis or whether there is cross-talk with necroptosis under these conditions. In this study, we report that Yersinia activates PANoptosis, as evidenced by the concerted activation of proteins involved in PANoptosis. Genetic deletion of RIPK1 abrogated the Yersinia-induced activation of the inflammasome/pyroptosis and apoptosis but enhanced necroptosis. We also found that Yersinia induced assembly of a RIPK1 PANoptosome complex capable of regulating all three branches of PANoptosis. Overall, our results demonstrate a role for the RIPK1 PANoptosome in Yersinia-induced inflammatory cell death and host defense.
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