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However, the mechanisms in relation to its expression compartment and enzymatic activity have not been completely explored. Moreover, only limited animal models have been studied to delineate its role at the tissue level in influenza infections. Our results showed that influenza A virus (IAV)-infected\n                    <jats:italic>\n                      Plscr1\n                      <jats:sup>-\/-<\/jats:sup>\n                    <\/jats:italic>\n                    mice exhibited exacerbated body weight loss, decreased survival rates, heightened viral replication, and increased lung damage. Interestingly, transcriptomic analyses demonstrated that Plscr1 was required for the expression of type 3 interferon receptor (Ifn-\u03bbr1) upon IAV infection by binding to its promoter. In addition, PLSCR1 interacted with IFN-\u03bbR1 on the cell surface of pulmonary epithelial cells following IAV infection, suggesting it also modulated IFN-\u03bb signaling via protein-protein interactions. The lipid scramblase activity of PLSCR1 was found to be dispensable for its anti-flu activity. Finally, single-cell RNA sequencing data indicated that\n                    <jats:italic>Plscr1<\/jats:italic>\n                    expression was significantly upregulated in ciliated airway epithelial cells in mice following IAV infection. Consistently,\n                    <jats:italic>\n                      Plscr1\n                      <jats:sup>floxStop<\/jats:sup>\n                      ;Foxj1-Cre\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:italic>\n                    mice with ciliated epithelial cell-specific Plscr1 overexpression showed reduced susceptibility to IAV infection, less inflammation, and enhanced Ifn-\u03bbr1 expression, suggesting that Plscr1 primarily regulates type 3 IFN signaling as a cell-intrinsic defense factor against IAV in ciliated airway epithelial cells. Our research will elucidate virus-host interactions and pave the way for the development of novel anti-influenza drugs that target human elements like PLSCR1, thereby mitigating the emergence of drug-resistant IAV strains.\n                  <\/jats:p>","DOI":"10.7554\/elife.104359","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T09:25:31Z","timestamp":1741685131000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.104359","source":"Crossref","is-referenced-by-count":1,"title":["Phospholipid scramblase 1 (PLSCR1) regulates interferon-lambda receptor 1 (IFN-\u03bbR1) and IFN-\u03bb signaling in influenza A virus (IAV) infection"],"prefix":"10.7554","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1528-9129","authenticated-orcid":true,"given":"Alina Xiaoyu","family":"Yang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05gq02987","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular 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