Sterile inflammation in the brain is recognized as a key component of many neurological diseases including multiple sclerosis (MS), amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease. An understanding of the mechanisms by which neuroinflammation occurs and the molecular mediators involved in this process is necessary for identification of potential therapeutic targets. The NLR gene family members have emerged as important regulators of immunity and inflammation due to their genetic linkage to several human immunologic diseases. In this study, our goal was to ascertain the role of NLR dependent cellular pathways in neuroinflammation, demyelination and remyelination. An in vivo cuprizone-induced mouse model of demyelination and remyelination along with ex vivo primary cell culture assays were utilized. Mice deficient in NLRP3 (Nlrp3-/-), IL-1[beta] (IL-1[beta]-/-), caspase-1 (casp1-/-), P2X7R (P2X7R-/-), IL-18 (IL-18-/-) and NLRC4 (Nlrc4-/-) were used for these studies
