We next questioned how TLR2 regulated allergic airway inflammation. It has been shown that NLRP3 inflammasome is associated with allergic airway disease in response to OVA (10). We next assessed the link between TLR2 and NLRP3 inflammasome activity. Our results showed that NLRP3, cleaved form of IL-1β and caspase 1(p20) were increased in OVA-challenged WT mice in comparison with those of control mice, while such increase was completely abrogated in TLR2−/− mice following OVA challenge (Figures 3A–D). Similarly, productions of NLRP3-associated IL-1β and IL-18 were markedly decreased in OVA-challenged TLR2−/− mice, comparable to those of control mice (Figures 3E,F). Taken together, in this OVA model, NLRP3 inflammasome activated by OVA required licensing through TLR2, suggesting that TLR2-NLRP3 axis mediated OVA-allergic airway inflammation.