IL1B and silicosis: Given that epithelial cells directly encounter inhaled silica particles and express NLRP3, we investigated the functional contribution of epithelial Nlrp3 to silicosis pathogenesis.<h4>Results</h4>Using inducible epithelial-specific knockout models, we found that alveolar epithelial (Sftpc<sup>+</sup>) cells drive early caspase-1 activation and airway IL-18 production, while partially reducing tissue IL-1β maturation.