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The aim of this study was to test whether the autoantibody profile in patients with myositis is associated with a type I interferon (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>) signature, as in patients with systemic lupus erythematous (<jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>). Patients with myositis were prospectively enrolled in the study and compared to healthy controls and to patients with <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>. Autoantibody status was analysed using an immunoassay system and immunoprecipitation. Type I <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> activity in whole blood was determined using direct gene expression analysis. Serum <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010inducing activity was tested using peripheral blood cells from healthy donors. Blocking experiments were performed by neutralizing anti\u2010<jats:styled-content style=\"fixed-case\">IFNAR<\/jats:styled-content> or anti\u2010<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> antibodies. Patients were categorized into <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> high and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> low based on an <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> score. Patients with autoantibodies against <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010binding proteins had a higher <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> score compared to patients without these antibodies, and the <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> score was related to autoantibody multispecificity. Patients with dermatomyositis (<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>) and inclusion body myositis (<jats:styled-content style=\"fixed-case\">IBM<\/jats:styled-content>) had a higher <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> score compared to the other subgroups. Serum type I <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> bioactivity was blocked by neutralizing anti\u2010<jats:styled-content style=\"fixed-case\">IFNAR<\/jats:styled-content> or anti\u2010<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> antibodies. To conclude, a high <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> score was not only associated with <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>, as previously reported, and <jats:styled-content style=\"fixed-case\">IBM<\/jats:styled-content>, but also with autoantibody monospecificity against several <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010binding proteins and with autoantibody multispecificity. These studies identify <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> in sera as a trigger for activation of the type I <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> pathway in peripheral blood and support <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010<jats:italic>\u03b1<\/jats:italic> as a possible target for therapy in these patients.<\/jats:p>","DOI":"10.1111\/sji.12449","type":"journal-article","created":{"date-parts":[[2016,5,13]],"date-time":"2016-05-13T07:22:57Z","timestamp":1463124177000},"page":"100-109","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Autoantibody Specificities and Type I Interferon Pathway Activation in Idiopathic Inflammatory Myopathies"],"prefix":"10.1111","volume":"84","author":[{"given":"L.","family":"Ekholm","sequence":"first","affiliation":[{"name":"Rheumatology Unit Department of Medicine Karolinska University Hospital Karolinska Institutet Solna Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Vosslamber","sequence":"additional","affiliation":[{"name":"Department of Pathology VU University Medical Center Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Tj\u00e4rnlund","sequence":"additional","affiliation":[{"name":"Rheumatology Unit Department of Medicine Karolinska University Hospital Karolinska Institutet Solna Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. 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