They further found that the pyrin 3 (NLRP3) domain of the (NOD)-like receptor (NLR), which is a key mediator in the production of IL-1 family cytokines in periodontitis, was targeted by miR-223-3p because when they eliminated miR-223-3p expression in THP-1-derived macrophages, the expression of NLRP3 and the inflammatory mediators IL-1β and IL-6 increased (46, 47). This evidence concerns the gene IL1B and periodontitis.