Indeed, consistent with our in vivo data, studies with WT and Trem2−/− BMDMs have reported an inherent hyperinflammatory phenotype of Trem2−/− BMDM in response to LPS (27) as well as an increased NLRP3 activation in the context of bacterial infection and neuro-inflammation (28, –30). This evidence concerns the gene NLRP3 and bacterial infectious disease.