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Nucleic acid and compact nucleic acid-like molecules can act as pathogen connected molecular patterns (PAMPs) to trigger variety I interferon (IFN-I) and also other cytokine induction (Takeuchi and Akira, 2007). Among DNA sensors, STING (also referred to as mediator of IRF3 activation (MITA), plasma membrane tetraspanner (MPYS) or endoplasmic reticulum IFN stimulator (ERIS) has emerged as central for DNA-induced IFN-I activation (Ishikawa et al., 2009; Jin et al., 2008; Sun et al., 2009; Zhong et al., 2008). Other DNA sensors like gamma-interferon-inducible protein 16 (IFI16) and DEAD (Asp-Glu-Ala-Asp) box polypeptide 41 (DDX41) are known to activate IFN-I in a STING-dependent manner (Unterholzner et al., 2010; Zhang et al., 2011). The nucleotide binding domain and leucine-rich repeat-containing (NLR) protein loved ones are intracellular sensors that regulate inflammatory responses (Eisenbarth and Flavell, 2009; Shaw et al., 2010). Most NLRs positively influence inflammatory responses, particularly the inflammasome NLRs. However emerging studies of gene-deficient mice have revealed that numerous NLRs negatively impact innate immune responses (Allen et al., 2011; Allen et al., 2012; Anand et al., 2012; Cui et al., 2010; Schneider et al., 2012; Xia et al., 2011; Zaki et al., 2011). Notably, we have previously shown that NLRC3 reduces LPS-induced nuclear factor kappa B (NF-B) activation by way of inhibiting the adaptor protein TNF receptor associated issue six (TRAF6)(Schneider et al., 2012). Having said that, the intersection of NLRs with DNA-sensing molecules has not been described. Within this report, we discover that NLRC3 deficiency also results in improved innate immune respon.
