tetano
Editor, Senior Moderator
Innate Immun. 2012 Dec 4. [Epub ahead of print]
NLRX1 does not inhibit MAVS-dependent antiviral signalling.
Soares F, Tattoli I, Wortzman ME, Arnoult D, Philpott DJ, Girardin SE.
Source
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Abstract
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.
PMID:
23212541
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23212541
NLRX1 does not inhibit MAVS-dependent antiviral signalling.
Soares F, Tattoli I, Wortzman ME, Arnoult D, Philpott DJ, Girardin SE.
Source
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Abstract
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.
PMID:
23212541
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23212541