NLRX1 does not inhibit MAVS-dependent antiviral signalling

被引:68
|
作者
Soares, Fraser [1 ]
Tattoli, Ivan [1 ,2 ]
Wortzman, Michael E. [2 ]
Arnoult, Damien [3 ]
Philpott, Dana J. [2 ]
Girardin, Stephen E. [1 ]
机构
[1] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON M5S 1A8, Canada
[2] Univ Toronto, Dept Immunol, Toronto, ON M5S 1A8, Canada
[3] Hop Paul Brousse, INSERM, U1014, Villejuif, France
基金
加拿大健康研究院;
关键词
Nod-like receptors; RIG-I like receptors; MAVS; innate immunity; NLRX1; NF-KAPPA-B; NOD-LIKE RECEPTOR; RIG-I; ADAPTER PROTEIN; IMMUNITY; VIRUS; PATHWAYS; INNATE; BETA; INFLAMMATION;
D O I
10.1177/1753425912467383
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:438 / 448
页数:11
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