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Critical role of Syk-dependent STAT1 activation in innate antiviral immunity.

Abstract：

:The JAK/STAT1 pathway is generally activated by cytokines, providing essential antiviral defense. Here, we identify that STAT1 activation is independent of cytokines and JAKs at the early infection stage of some viruses, including influenza A virus (IAV). Instead, STAT1 is activated mainly through spleen tyrosine kinase (Syk) downstream of retinoic acid-inducible gene-I/mitochondrial antiviral-signaling protein (RIG-I/MAVS) signaling. Syk deletion profoundly impairs immediate innate immunity, as evidenced by the finding that Syk deletion attenuates tyrosine phosphorylation of STAT1 and reduces the expressions of interferon-stimulated genes (ISGs) in vitro and in vivo. The antiviral response to IAV infection is also significantly suppressed in the STAT1Y701F knockin mice. The results demonstrate that STAT1 activation is dependent on Syk rather than the cytokine-activated JAK signaling at the early stage of viral infection, which is critical for initial antiviral immunity. Our finding provides insights into the complicated mechanisms underlying host immune responses to viral infection.

journal_name

Cell Rep

journal_title

Cell reports

authors

Liu S,Liao Y,Chen B,Chen Y,Yu Z,Wei H,Zhang L,Huang S,Rothman PB,Gao GF,Chen JL

doi

10.1016/j.celrep.2020.108627

subject

Has Abstract

pub_date

2021-01-19 00:00:00

pages

108627

issue

3

issn

2211-1247

pii

S2211-1247(20)31616-8

journal_volume

34

pub_type

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