{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T05:23:12Z","timestamp":1787721792551,"version":"build-2784847793"},"reference-count":54,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T00:00:00Z","timestamp":1773705600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T00:00:00Z","timestamp":1773705600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100018208","name":"Cure JM Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100018208","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100015391","name":"Myositis Association","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100015391","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Arthritis &amp;amp; Rheumatology"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Dysregulated type I interferon (IFN) signaling contributes to autoimmune myositis pathogenesis. We investigated the therapeutic effects of JAK inhibitors in two mouse models. We also examined how type I IFNs affect muscle vasculature.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Myositis was induced in major histocompatibility complex class I double transgenic ([TRE\u2010H\u20102K\n                      <jats:sup>b<\/jats:sup>\n                      (H mice)\/MCK\u2010tTA (T mice)] (HT)) female mice at day 21. Mice were randomized into four groups (n\u00a0=\u00a010\u201311\/group): baricitinib (10 mg\/kg), tofacitinib (20 mg\/kg), vehicle, and healthy controls. Outcomes included survival, weight, muscle strength, histopathology, and IFN\u2010stimulated gene expression. To model IFN\u03b2 overexpression, C57BL\/6 mice received AAV9\u2010triple muscle\u2010specific creatine kinase (tMCK)\u2010IFN\u03b2 and were treated with vehicle or tofacitinib (40 mg\/kg\/day) for 10 weeks (n\u00a0=\u00a08\u201313\/group).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Tofacitinib\u2014but not baricitinib\u2014significantly reduced IFN scores in mice with severe myositis (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.05). Survival differed across groups (overall log\u2010rank\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01), with untreated\u2010 and baricitinib\u2010treated HT mice showing shorter survival than BL\/6 controls, whereas tofacitinib\u2010treated mice did not differ from controls. IFN\u03b2 overexpression induced muscle inflammation (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01), reduced grip strength (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.0001), and increased the IFN score (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.0001) and H2Kb (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.0001) expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Tofacitinib reduced the IFN signature, and survival in this group did not differ significantly from healthy controls, whereas untreated and baricitinib\u2010treated HT mice showed shorter survival; functional improvement was not observed. Our results also show that type I IFN signaling contributes to muscle inflammation and weakness, making it a key driver of muscle damage and thereby reinforcing its potential as a therapeutic target.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art70096-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  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