Importantly, our study shows for the first time that the exaggerated airway inflammation observed in CIA + LPS mice is accompanied by increases in profibrotic mediators (i.e., MMP-8, MMP-9, TIMP-1, IL-33, and C5a), activated CD11c+CD11b+ macrophages, recruited/transitioning CD11cintCD11b+ monocytes-macrophages, neutrophils, NETosis, and increased expression of MAA- and CIT-modified proteins, lung autoantigens that have been implicated in the pathogenesis of RA and RA-ILD (19). The gene discussed is IL33; the disease is interstitial lung disease.