{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T13:16:13Z","timestamp":1792674973111,"version":"4.5.0"},"reference-count":60,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,6,8]],"date-time":"2012-06-08T00:00:00Z","timestamp":1339113600000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:p>Polymorphisms in the transcription factor interferon (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>) regulatory factor 5 (<jats:italic><jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5<\/jats:italic>) have been identified that show a strong association with an increased risk of developing the autoimmune disease systemic lupus erythematosus (<jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>). A potential pathological role for <jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5 in <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> development is supported by the fact that increased <jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5 m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and protein are observed in primary blood cells of <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> patients and this correlates with an increased risk of developing the disease. Here, we demonstrate that <jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5 is required for pristane\u2010induced <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> via its ability to control multiple facets of autoimmunity. We show that <jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5 is required for pathological hypergammaglobulinemia and, in the absence of <jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5, <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>g<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content> class switching is reduced. Examination of in vivo cytokine expression (and autoantibody production) identified an increase in <jats:italic><jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>rf5<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h2 cytokines. In addition, we provide clear evidence that loss of <jats:italic><jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>rf5<\/jats:italic> significantly weakens the in vivo type I <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> signature critical for disease pathogenesis in this model of murine lupus. Together, these findings demonstrate the importance of <jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5 for autoimmunity and provide a significant new insight into how overexpression of <jats:styled-content style=\"fixed-case\">IRF<\/jats:styled-content>5 in blood cells of <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> patients may contribute to disease pathogenesis.<\/jats:p>","DOI":"10.1002\/eji.201141642","type":"journal-article","created":{"date-parts":[[2012,6,8]],"date-time":"2012-06-08T11:28:19Z","timestamp":1339154899000},"page":"1477-1487","source":"Crossref","is-referenced-by-count":68,"title":["<i><scp>I<\/scp>rf5<\/i>\u2010deficient mice are protected from pristane\u2010induced lupus via increased <scp>T<\/scp>h2 cytokines and altered <scp>I<\/scp>g<scp>G<\/scp> class switching"],"prefix":"10.1002","volume":"42","author":[{"given":"Di","family":"Feng","sequence":"first","affiliation":[{"name":"Department of Biochemistry &amp; Molecular Biology New Jersey Medical School UMDNJ  Newark NJ USA"},{"name":"New Jersey Medical School\u2010University Hospital Cancer Center UMDNJ  Newark NJ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisong","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Biochemistry &amp; Molecular Biology New Jersey Medical School UMDNJ  Newark NJ USA"},{"name":"New Jersey Medical School\u2010University Hospital Cancer Center UMDNJ  Newark NJ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohui","family":"Bi","sequence":"additional","affiliation":[{"name":"Department of Biochemistry &amp; Molecular Biology New Jersey Medical School UMDNJ  Newark NJ USA"},{"name":"New Jersey Medical School\u2010University Hospital Cancer Center UMDNJ  Newark NJ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rivka C.","family":"Stone","sequence":"additional","affiliation":[{"name":"Department of Biochemistry &amp; Molecular Biology New Jersey Medical School UMDNJ  Newark NJ USA"},{"name":"New Jersey Medical School\u2010University Hospital Cancer Center UMDNJ  Newark NJ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Priya","family":"Patel","sequence":"additional","affiliation":[{"name":"New Jersey Medical School\u2010University Hospital Cancer Center UMDNJ  Newark NJ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Betsy J.","family":"Barnes","sequence":"additional","affiliation":[{"name":"Department of Biochemistry &amp; Molecular Biology New Jersey Medical School UMDNJ  Newark NJ USA"},{"name":"New Jersey Medical School\u2010University Hospital Cancer Center UMDNJ  Newark NJ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,6,8]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra071297"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1586\/eci.10.8"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrrheum.2010.63"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrg2571"},{"key":"e_1_2_6_6_1","unstructured":"Cohen P. 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