{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,4]],"date-time":"2026-07-04T21:23:07Z","timestamp":1783200187520,"version":"3.54.6"},"reference-count":50,"publisher":"BMJ","issue":"7","license":[{"start":{"date-parts":[[2025,8,1]],"date-time":"2025-08-01T00:00:00Z","timestamp":1754006400000},"content-version":"unspecified","delay-in-days":1,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000738","name":"US Department of Veterans Affairs","doi-asserted-by":"crossref","award":["I01CX001364"],"award-info":[{"award-number":["I01CX001364"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["R01CA264983"],"award-info":[{"award-number":["R01CA264983"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["R01CA278852"],"award-info":[{"award-number":["R01CA278852"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["R43 CA250780"],"award-info":[{"award-number":["R43 CA250780"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2025,7,16]]},"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Emerging clinical and mouse tumor data indicate that tumor cells induce immune suppression in an anatomical site-specific manner. In lung metastases, tumor cell programmed death-ligand 1 (PD-L1) engages myeloid cell programmed cell death protein 1 to activate SHP2 to suppress type I interferon (IFN-I) expression to repress Cxcl9 expression to impair cytotoxic T lymphocyte (CTL) tumor recruitment. Loss of IFN-I expression thus underlies tumor immune evasion in lung metastases niche. We aimed at testing the hypothesis that forcing tumor cells to express IFN\u03b12 activates Cxcl9 expression to increase CTL tumor recruitment to suppress lung metastasis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Codon usage-optimized IFN\u03b12-encoding DNA was designed and cloned to plasmid. IFN\u03b12-encoding messenger RNA (mRNA) was synthesized. The plasmid DNA and mRNA were encapsulated into DOTAP (N-[1-(2,3-Dioleoyloxy)propyl]-N,N,N-trimethylammonium methyl-sulfate)-cholesterol to generate lipid nanoparticle (LNP)-encapsulated mouse IFN\u03b12 (LNP-mIFN\u03b12), human IFN\u03b12 plasmid, and mouse IFN\u03b12 mRNA (LNP-mIFN\u03b12-mRNA). Mouse breast tumor spontaneous lung metastasis, mouse melanoma experimental lung metastasis, and human colon tumor experimental lung metastasis humanized mouse models were used to determine LNP-encapsulated IFN\u03b12-encoding plasmid and mRNA efficacy in IFN\u03b12 expression and antitumor immunity, toxicity, and mechanism of action in vivo.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>LNP-encapsulated IFN\u03b12-encoding plasmid primarily accumulated in tumor-bearing lungs in mice. LNP-IFN\u03b12 therapy produces mouse IFN\u03b12 protein in mouse tumor-bearing mice and human IFN\u03b12 protein in human tumor-bearing humanized mice to suppress lung metastasis, respectively. Similarly, LNP-mIFN\u03b12-mRNA therapy produces mouse IFN\u03b12 protein and suppressed lung metastasis in tumor-bearing mice. The increased IFN\u03b12 protein activates Cxcl9 expression and increases T cell infiltration in lung metastases. LNP-IFN\u03b12 therapy did not induce liver toxicity and inflammatory cytokines. In human patients with cancer, IFN-I pathway activation is correlated with CXCL9 expression and T cell expansion after PD-(L)1 immune checkpoint inhibitor immunotherapy. Mechanistically, LNP-delivered IFN\u03b12 suppresses tumor lung metastasis through upregulating Cxcl9 in tumor-bearing mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings determine that LNP-encapsulated IFN\u03b12-encoding plasmid DNA and mRNA are effective agents in restoring IFN\u03b12 expression to activate Cxcl9 expression to enhance T cell tumor recruitment to suppress tumor lung metastasis. LNP-IFN\u03b12 is potentially a safe and yet effective third-generation IFN\u03b12 agent for human cancer immunotherapy to treat patients with lung metastasis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2024-011415","type":"journal-article","created":{"date-parts":[[2025,8,1]],"date-time":"2025-08-01T06:20:23Z","timestamp":1754029223000},"page":"e011415","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Lipid nanoparticle-delivered IFN\u03b12 activates Cxcl9 to increase T cell tumor recruitment to suppress lung 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