POH1 deubiquitinates pro-interleukin-1β and restricts inflammasome activity

Li Zhang, Yun Liu, Boshi Wang, Guiqin Xu, Zhaojuan Yang, Ming Tang, Aihui Ma, Tiantian Jing, Xiaoli Xu, Xiaoren Zhang and Yongzhong Liu ()
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Li Zhang: Shanghai Jiao Tong University School of Medicine
Yun Liu: Shanghai Jiao Tong University School of Medicine
Boshi Wang: Shanghai Jiao Tong University School of Medicine
Guiqin Xu: Shanghai Jiao Tong University School of Medicine
Zhaojuan Yang: Shanghai Jiao Tong University School of Medicine
Ming Tang: Shanghai Jiao Tong University School of Medicine
Aihui Ma: Shanghai Jiao Tong University School of Medicine
Tiantian Jing: Shanghai Jiao Tong University School of Medicine
Xiaoli Xu: Shanghai Jiao Tong University School of Medicine
Xiaoren Zhang: Chinese Academy of Sciences (CAS)
Yongzhong Liu: Shanghai Jiao Tong University School of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Inflammasome activation is essential for host defence against invading pathogens, but is also involved in various forms of inflammatory diseases. The processes that control inflammasome activity are thus important for averting excessive immune responses and tissue damage. Here we show that the deubiquitinase POH1 negatively regulates the immune response triggered by inflammasome activation. POH1 deficiency in macrophages enhances mature IL-1β production without significant alterations in inflammasome priming and ASC-caspase-1 activation. In WT macrophages, POH1 interacts with and deubiquitinates pro-IL-1β by decreasing the K63-linked polyubiquitin chains, as well as decreases the efficacy of pro-IL-1β cleavage. Furthermore, myeloid cell-specific deletion of POH1 aggravates lipopolysaccharide-induced systemic inflammation and alum-induced peritonitis inflammatory responses in vivo. Our study thereby reveals that POH1-mediated deubiquitination of pro-IL-1β is an important regulatory event that restrains inflammatory responses for the maintenance of immune homeostasis.

Date: 2018
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DOI: 10.1038/s41467-018-06455-z

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