NLRX1 does not inhibit MAVS-dependent antiviral signalling

NLRX1 is a member of the Nod-like receptor family of intracellular sensors of microbial- and danger-associated molecular patterns. NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with r...

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Bibliographic Details
Published in:Innate immunity (London, England) England), 2013-08, Vol.19 (4), p.438-448
Main Authors: Soares, Fraser, Tattoli, Ivan, Wortzman, Michael E, Arnoult, Damien, Philpott, Dana J, Girardin, Stephen E
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - metabolism
Animals
Cell Line
Chemokine CXCL10 - genetics
Chemokine CXCL10 - metabolism
Fibroblasts - immunology
Immunity, Innate
Inflammation Mediators - metabolism
Influenza A virus
Influenza A virus - immunology
Interleukin-6 - genetics
Interleukin-6 - metabolism
Macrophages - immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Orthomyxoviridae Infections - immunology
Poly I-C - immunology
Respirovirus Infections - immunology
Sendai virus
Sendai virus - immunology
Signal Transduction
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Summary:NLRX1 is a member of the Nod-like receptor family of intracellular sensors of microbial- and danger-associated molecular patterns. NLRX1 has a N-terminal mitochondrial addressing sequence that localizes the protein to the mitochondrial matrix. Recently, conflicting reports have been presented with regard to the putative implication of NLRX1 as a negative regulator of MAVS-dependent cytosolic antiviral responses. Here, we generated a new NLRX1 knockout mouse strain and observed that bone marrow-derived macrophages and murine embryonic fibroblasts from NLRX1-deficient mice displayed normal antiviral and inflammatory responses following Sendai virus infection. Importantly, wild type and NLRX1-deficient mice exhibited unaltered antiviral and inflammatory gene expression following intranasal challenge with influenza A virus or i.p. injection of Poly (I:C). Together, our results demonstrate that NLRX1 does not participate in the negative regulation of MAVS-dependent antiviral responses.
ISSN:1753-4259
1753-4267
DOI:10.1177/1753425912467383