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Here, we demonstrate that type I interferon (IFN-I) signaling primes the lung for alveolar renewal following viral challenge. IFN-I contributes to the induction of an interferon-stimulated gene-high (ISG)\n                  <jats:sup>hi<\/jats:sup>\n                  Sca-1\n                  <jats:sup>Pos<\/jats:sup>\n                  population of alveolar type II (ATII) epithelial cells. Sca-1\n                  <jats:sup>Pos<\/jats:sup>\n                  ATIIs exhibit enhanced proliferative capacity and increased organoid-forming efficiency compared with their Sca-1\n                  <jats:sup>Neg<\/jats:sup>\n                  counterparts. Viral challenge concurrently drives phenotypic reprogramming of tissueresident alveolar macrophages (trAMs). Sca-1\n                  <jats:sup>Pos<\/jats:sup>\n                  ATIIs display heightened responsiveness to oncostatin M (OSM) and, following viral challenge, require trAM-derived OSM for their proliferation. Together, these findings reveal that viral stimuli induce coordinated IFN-I-dependent epithelial and macrophage states that poise the lung for regeneration, positioning IFN-I not only as a central antiviral defense mechanism but as a priming signal that prepares lung tissue for renewal.\n                <\/jats:p>","DOI":"10.64898\/2026.06.10.731366","type":"posted-content","created":{"date-parts":[[2026,6,13]],"date-time":"2026-06-13T01:20:20Z","timestamp":1781313620000},"source":"Crossref","is-referenced-by-count":0,"title":["Type I interferon primes the alveolar epithelium to receive reparative signals from tissue-resident macrophages"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5768-1271","authenticated-orcid":false,"given":"Alan Y.","family":"Baez Vazquez","sequence":"first","affiliation":[{"name":"Department of Immunology, Harvard Medical School, Boston, MA, USA"},{"name":"Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, 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