NLRX1 does not inhibit MAVS-dependent antiviral signalling.

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Innate immunity 2012 Dec 4. [Epub ahead of print]

NLRX1 does not inhibit MAVS-dependent antiviral signalling.

F Soares;I Tattoli;ME Wortzman;D Arnoult;DJ Philpott;SE Girardin

Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.

Service type: Knockout mice


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.

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