PLCβ2 negatively regulates the inflammatory response to virus infection by inhibiting phosphoinositide-mediated activation of TAK1 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Lin Wang, Yilong Zhou, Zijuan Chen, Lei Sun, Juehui Wu, Haohao Li, Feng Liu, Fei Wang, Chunfu Yang, Juhao Yang, Qibin Leng, Qingli Zhang, Ajing Xu, Lisong Shen, Jinqiao Sun, Dianqing Wu, Caiyun Fang, Haojie Lu, Dapeng Yan, Baoxue Ge

ABSTRACT

Excessive or uncontrolled release of proinflammatory cytokines caused by severe viral infections often results in host tissue injury or even death. Phospholipase C (PLC)s degrade phosphatidylinositol-4, 5-bisphosphate (PI(4,5)P2) lipids and regulate multiple cellular events. Here, we report that PLCβ2 inhibits the virus-induced expression of pro-inflammatory cytokines by interacting with and inhibiting transforming growth factor-β-activated kinase 1 (TAK1) activation. Mechanistically, PI(4,5)P2 lipids directly interact with TAK1 at W241 and N245, and promote its activation. Impairing of PI(4,5)P2's binding affinity or mutation of PIP2-binding sites on TAK1 abolish its activation and the subsequent production of pro-inflammatory cytokines. Moreover, PLCβ2-deficient mice exhibit increased expression of proinflammatory cytokines and a higher frequency of death in response to virus infection, while the PLCβ2 activator, m-3M3FBS, protects mice from severe Coxsackie virus A 16 (CVA16) infection. Thus, our findings suggest that PLCβ2 negatively regulates virus-induced pro-inflammatory responses by inhibiting phosphoinositide-mediated activation of TAK1. More... »

PAGES

746

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41467-019-08524-3

DOI

http://dx.doi.org/10.1038/s41467-019-08524-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1112133871

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30765691


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