NDLI: Induction of PGRN by influenza virus inhibits the antiviral immune responses through downregulation of type I interferons signaling

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Induction of PGRN by influenza virus inhibits the antiviral immune responses through downregulation of type I interferons signaling

Content Provider	Semantic Scholar
Author	Wei, Fanhua Jiang, Zhimin Sun, Honglei Pu, Juan Sun, Yipeng Wang, Mingyang Tong, Qi Bi, Yuhai Ma, Xiaojing Gao, George Fu Liu, Jin-Hua
Copyright Year	2019
Abstract	Type I interferons (IFNs) play a critical role in host defense against influenza virus infection, and the mechanism of influenza virus to evade type I IFNs responses remains to be fully understood. Here, we found that progranulin (PGRN) was significantly increased both in vitro and in vivo during influenza virus infection. Using a PGRN knockdown assay and PGRN-deficient mice model, we demonstrated that influenza virus-inducing PGRN negatively regulated type I IFNs production by inhibiting the activation of NF-κB and IRF3 signaling. Furthermore, we showed that PGRN directly interacted with NF-κB essential modulator (NEMO) via its Grn CDE domains. We also verified that PGRN recruited A20 to deubiquitinate K63-linked polyubiquitin chains on NEMO at K264. In addition, we found that macrophage played a major source of PGRN during influenza virus infection, and PGRN neutralizing antibodies could protect against influenza virus-induced lethality in mice. Our data identify a PGRN-mediated IFN evasion pathway exploited by influenza virus with implication in antiviral applications. These findings also provide insights into the functions and crosstalk of PGRN in innate immunity.
File Format	PDF HTM / HTML
DOI	10.1371/journal.ppat.1008062
PubMed reference number	31585000
Journal	Medline
Volume Number	15
Alternate Webpage(s)	https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1008062&type=printable
Alternate Webpage(s)	https://doi.org/10.1371/journal.ppat.1008062
Journal	PLoS pathogens
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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