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Despite the rarity of each of the fibrotic ILDs individually, they cumulatively affect a considerable number of patients. PPF is characterised by an excessive collagen deposition leading to functional decline.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Therapeutic options are limited to nintedanib and pirfenidone which are only able to reduce fibrosis progression. CD206-expressing M2 macrophages are involved in fibrosis progression, and whether they may be relevant therapeutic targets or biomarkers remains an open question.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In our study, CD206\n                      <jats:sup>+<\/jats:sup>\n                      lung macrophages were monitored in bleomycin-induced lung fibrosis in mice by combining flow cytometry, scRNAseq and in vivo molecular imaging using a single photon emission computed tomography (SPECT) radiopharmaceutical,\n                      <jats:sup>99m<\/jats:sup>\n                      Tc-tilmanocept. The antifibrotic effect of the inhibition of M2 macrophage polarisation with a JAK inhibitor, tofacitinib, was assessed in vivo. We demonstrate that CD206-targeted in vivo SPECT imaging with\n                      <jats:sup>99m<\/jats:sup>\n                      Tc-tilmanocept was able to accurately detect and quantify the increase in CD206\n                      <jats:sup>+<\/jats:sup>\n                      macrophages from early to advanced stages of experimental fibrosis and ex vivo in lung biopsies from patients with IPF. CD206-targeted imaging also specifically detected a decrease in CD206\n                      <jats:sup>+<\/jats:sup>\n                      lung macrophages on nintedanib and tofacitinib treatment. Importantly, early in vivo imaging of CD206\n                      <jats:sup>+<\/jats:sup>\n                      macrophages allowed the prediction of experimental lung fibrosis progression as well as nintedanib and tofacitinib efficacy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings indicate that M2 macrophages may be relevant theranostic targets for personalised medicine for patients with PPF.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/thorax-2023-221168","type":"journal-article","created":{"date-parts":[[2024,7,22]],"date-time":"2024-07-22T04:32:48Z","timestamp":1721622768000},"page":"1124-1135","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":23,"title":["CD206\n                    <sup>+<\/sup>\n                    macrophages are relevant non-invasive imaging biomarkers and therapeutic targets in experimental lung fibrosis"],"prefix":"10.1136","volume":"79","clinical-trial-number":[{"clinical-trial-number":"nct05246293","registry":"10.18810\/clinical-trials-gov"},{"clinical-trial-number":"nct04311567","registry":"10.18810\/clinical-trials-gov"},{"clinical-trial-number":"nct04311567","registry":"10.18810\/clinical-trials-gov"},{"clinical-trial-number":"nct05246293","registry":"10.18810\/clinical-trials-gov"}],"author":[{"given":"Lenny","family":"Pommerolle","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2830-5642","authenticated-orcid":false,"given":"Guillaume","family":"Beltramo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leo","family":"Biziorek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marin","family":"Truchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandre 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