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NLRX1 promotes immediate IRF1-directed antiviral responses by limiting dsRNA-activated translational inhibition mediated by PKR.

Abstract：

:NLRX1 is unique among the nucleotide-binding-domain and leucine-rich-repeat (NLR) proteins in its mitochondrial localization and ability to negatively regulate antiviral innate immunity dependent on the adaptors MAVS and STING. However, some studies have suggested a positive regulatory role for NLRX1 in inducing antiviral responses. We found that NLRX1 exerted opposing regulatory effects on viral activation of the transcription factors IRF1 and IRF3, which might potentially explain such contradictory results. Whereas NLRX1 suppressed MAVS-mediated activation of IRF3, it conversely facilitated virus-induced increases in IRF1 expression and thereby enhanced control of viral infection. NLRX1 had a minimal effect on the transcription of IRF1 mediated by the transcription factor NF-kB and regulated the abundance of IRF1 post-transcriptionally by preventing translational shutdown mediated by the double-stranded RNA (dsRNA)-activated kinase PKR and thereby allowed virus-induced increases in the abundance of IRF1 protein.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Feng H,Lenarcic EM,Yamane D,Wauthier E,Mo J,Guo H,McGivern DR,González-López O,Misumi I,Reid LM,Whitmire JK,Ting JP,Duncan JA,Moorman NJ,Lemon SM

doi

10.1038/ni.3853

subject

Has Abstract

pub_date

2017-12-01 00:00:00

pages

1299-1309

issue

12

eissn

1529-2908

issn

1529-2916

pii

ni.3853

journal_volume

18

pub_type

杂志文章

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