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The pathogenesis of PF-ILDs involves macrophages driving inflammation and irreversible fibrosis. Fc-\u03b3 receptors (Fc\u03b3Rs) regulate macrophages and inflammation, but their roles in PF-ILDs remain unclear. We characterized the expression of Fc\u03b3Rs and found upregulated Fc\u03b3RIIB in human and mouse lungs after exposure to silica. Fc\u03b3RIIB deficiency aggravated lung dysfunction, inflammation, and fibrosis in silica-exposed mice. Using single-cell transcriptomics and in vitro experiments, Fc\u03b3RIIB was found in alveolar macrophages, where it regulated the expression of fibrosis-related genes Spp1 and Ctss. In mice with macrophage-specific overexpression of Fc\u03b3RIIB and in mice treated with adenovirus by intratracheal instillation to upregulate Fc\u03b3RIIB, silica-induced functional and histological changes were ameliorated. Our data from three genetic models and a therapeutic model suggest that Fc\u03b3RIIB plays a protective role that can be enhanced by adenoviral overexpression, representing a potential therapeutic strategy for PF-ILDs.<\/jats:p>","DOI":"10.1165\/rcmb.2022-0056oc","type":"journal-article","created":{"date-parts":[[2022,10,13]],"date-time":"2022-10-13T13:31:48Z","timestamp":1665667908000},"page":"213-227","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":6,"title":["Adenovirus-mediated Overexpression of Fc\u03b3RIIB Attenuates Pulmonary Inflammation and Fibrosis"],"prefix":"10.1093","volume":"68","author":[{"given":"Zhe","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Pulmonary and Critical Care Medicine, The First Hospital of Shanxi Medical University, Taiyuan, China"},{"name":"Department of Physiology and"},{"name":"Department of Pathophysiology, State Key Laboratory of Medical Molecular Biology, 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