上睑下垂
磷脂酰肌醇
细胞生物学
炎症体
磷酸酶
化学
泛素
生物
免疫系统
磷脂酶D
生物化学
信号转导
免疫学
磷酸化
受体
基因
作者
Qiyao Chai,Shanshan Yu,Yanzhao Zhong,Zhe Lü,Changgen Qiu,Yang Yu,Xinwen Zhang,Yong Zhang,Zehui Lei,Lihua Qiang,Bing-Xi Li,Yu Pang,Xiao‐Bo Qiu,Jing Wang,Cui Hua Liu
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2022-10-13
卷期号:378 (6616)
被引量:76
标识
DOI:10.1126/science.abq0132
摘要
The inflammasome-mediated cleavage of gasdermin D (GSDMD) causes pyroptosis and inflammatory cytokine release to control pathogen infection, but how pathogens evade this immune response remains largely unexplored. Here we identify the known protein phosphatase PtpB from Mycobacterium tuberculosis as a phospholipid phosphatase inhibiting the host inflammasome-pyroptosis pathway. Mechanistically, PtpB dephosphorylated phosphatidylinositol-4-monophosphate and phosphatidylinositol-(4,5)-bisphosphate in host cell membrane, thus disrupting the membrane localization of the cleaved GSDMD to inhibit cytokine release and pyroptosis of macrophages. Notably, this phosphatase activity requires PtpB binding to ubiquitin. Disrupting phospholipid phosphatase activity or the ubiquitin-interacting motif of PtpB enhanced host GSDMD-dependent immune responses and reduced intracellular pathogen survival. Thus, pathogens inhibit pyroptosis and counteract host immunity by altering host membrane composition.
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