{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T09:33:20Z","timestamp":1771666400856,"version":"3.50.1"},"reference-count":46,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2005,6,28]],"date-time":"2005-06-28T00:00:00Z","timestamp":1119916800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2005,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To analyze the clinical and biologic correlates of autoantibody induction during longer\u2010term tumor necrosis factor \u03b1 (TNF\u03b1) blockade with either the monoclonal antibody infliximab or the soluble receptor etanercept.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Thirty\u2010four patients with spondylarthropathy (SpA) and 59 patients with rheumatoid arthritis (RA) were treated with infliximab for 2 years. Additionally, 20 patients with SpA were treated with etanercept for 1 year. Sera were blindly analyzed for antinuclear antibodies (ANAs), anti\u2013double\u2010stranded DNA (anti\u2010dsDNA) antibodies, anti\u2013extractable nuclear antigen (anti\u2010ENA) antibodies, and antihistone, antinucleosome, and anticardiolipin antibodies (aCL). The anti\u2010dsDNA antibodies were isotyped.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>High numbers of infliximab\u2010treated patients with SpA or RA had newly induced ANAs (61.8% and 40.7%, respectively) and anti\u2010dsDNA antibodies (70.6% and 49.2%, respectively) after 1 year, but no further increase between year 1 and year 2 was observed. In contrast, induction of ANAs and anti\u2010dsDNA antibodies was observed only occasionally in the etanercept\u2010treated patients with SpA (10% of patients each). Isotyping revealed almost exclusively IgM or IgM\/IgA anti\u2010dsDNA antibodies, which disappeared upon interruption of treatment. Neither infliximab nor etanercept induced other lupus\u2010related reactivities such as anti\u2010ENA antibodies, antihistone antibodies, or antinucleosome antibodies, and no clinically relevant lupus\u2010like symptoms were observed. Similarly, infliximab but not etanercept selectively increased IgM but not IgG aCL titers.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The prominent ANA and anti\u2010dsDNA autoantibody response is not a pure class effect of TNF\u03b1 blockers, is largely restricted to short\u2010term IgM responses, and is not associated with other serologic or clinical signs of lupus. Similar findings with aCL suggest that modulation of humoral immunity may be a more general feature of infliximab treatment.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.21190","type":"journal-article","created":{"date-parts":[[2005,6,28]],"date-time":"2005-06-28T14:49:57Z","timestamp":1119970197000},"page":"2192-2201","source":"Crossref","is-referenced-by-count":131,"title":["Infliximab, but not etanercept, induces IgM anti\u2013double\u2010stranded DNA autoantibodies as main antinuclear reactivity: Biologic and clinical implications in autoimmune arthritis"],"prefix":"10.1002","volume":"52","author":[{"given":"Leen","family":"de Rycke","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dominique","family":"Baeten","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elli","family":"Kruithof","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Filip","family":"Van den Bosch","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric M.","family":"Veys","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Filip","family":"de Keyser","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,6,28]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(94)90628-9"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1297-319X(01)00335-9"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.2174\/1568010023344535"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1186\/ar995"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.2165\/00019053-200422001-00005"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(99)05246-0"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1002\/1529-0131(200011)43:11<2383::AID-ANR2>3.0.CO;2-D"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.10876"},{"key":"e_1_2_6_10_2","first-page":"2557","article-title":"Induction of autoantibodies during prolonged treatment with infliximab","volume":"30","author":"Louis M","year":"2003","journal-title":"J Rheumatol"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1186\/ar1173"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2004.024182"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1186\/ar1440"},{"key":"e_1_2_6_14_2","unstructured":"Remicade[package insert]. 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