JT002 showed activity in both acute and chronic models, with the results indicating that NLRP3 inflammasome activation plays a critical role in IL-17-dependent neutrophilic asthma and ozone-induced airway inflammation and supports the notion that targeting NLRP3 with JT002 is a valid approach in treating severe, steroid-resistant neutrophilic asthma. Here, IL17A is linked to inflammatory response.