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Here we investigate the role of moMac-derived Pdgfa in bleomycin-induced lung fibrosis in mice. Deletion of Pdgfa with Cx3cr1-CreERT2 decreased bleomycin-induced lung fibrosis. Among a panel of in vitro macrophage polarizing stimuli, robust induction of Pdgfa was noted with IL10 in both mouse and human moMacs. Likewise, analysis of single-cell data revealed high expression of the receptor IL10RA in moMacs from human fibrotic lungs. Studies with IL10-GFP mice revealed that IL10-expressing cells were increased after injury in mice and colocalized with moMacs. Notably, deletion of IL10ra with Csf1r-Cre: IL10ra fl\/fl mice decreased both Pdgfa expression in moMacs and lung fibrosis. Taken together, these findings reveal a novel, IL10-dependent mechanism of macrophage polarization leading to fibroblast activation after injury. <\/jats:p>","DOI":"10.1152\/ajplung.00458.2021","type":"journal-article","created":{"date-parts":[[2022,2,2]],"date-time":"2022-02-02T13:00:42Z","timestamp":1643806842000},"page":"L495-L502","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":28,"title":["IL10 trains macrophage profibrotic function after lung injury"],"prefix":"10.1152","volume":"322","author":[{"given":"Aritra","family":"Bhattacharyya","sequence":"first","affiliation":[{"name":"Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California, San Francisco, California"},{"name":"Sandler Asthma Basic Research Center, University of California, San Francisco, 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