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A similar situation is seen in rheumatoid arthritis (RA) with both anti\u2010citrullinated protein antibodies (ACPA) and auto\u2010antibodies against the citrullinating enzyme, peptidylarginine deiminase (PAD). Previously, we have suggested that a complex between an enzyme and its modified substrate constitutes the neoantigen in autoimmune diseases. Our hypothesis is challenged by findings in patients of primary Sj\u00f6gren\u2019s syndrome (pSS) who do not express ACPA, but who have been reported to carry anti\u2010PAD. The aims of our investigation were to reproduce the study claiming the presence of anti\u2010PAD in pSS and screen for ACPA and antibodies against TG2 and PAD in pSS (<jats:italic>n<\/jats:italic>\u2003=\u200378), multiple sclerosis (MS) (<jats:italic>n<\/jats:italic>\u2003=\u200385) and Alzheimer's disease (AD) (<jats:italic>n<\/jats:italic>\u2003=\u200379) using ELISA. With blood donors (<jats:italic>n<\/jats:italic>\u2003=\u2003100) as controls, no increased occurrence of autoantibodies was found among the patient groups tested. Contrary to what has been published previously, patients with pSS do not express anti\u2010PAD. The hypothesis of a complex between an enzyme and its modified substrate constituting the neoantigen in autoimmune diseases is still valid. The prevalence of anti\u2010PAD, anti\u2010TG2 and ACPA is comparatively restricted. PAD and TG2 do not seem to be involved directly in autoimmune mechanisms in pSS, MS or AD.<\/jats:p>","DOI":"10.1111\/j.1365-3083.2008.02115.x","type":"journal-article","created":{"date-parts":[[2008,5,8]],"date-time":"2008-05-08T16:41:56Z","timestamp":1210264916000},"page":"626-631","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Pathogenesis of Autoimmune Diseases: Antibodies Against Transglutaminase, Peptidylarginine Deiminase and Protein\u2010bound Citrulline in Primary Sj\u00f6gren\u2019s Syndrome, Multiple Sclerosis and Alzheimer\u2019s Disease"],"prefix":"10.1111","volume":"67","author":[{"given":"E.","family":"Bodil Roth","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.","family":"Theander","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.","family":"Londos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Sandberg\u2010Wollheim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"\u00c5.","family":"Larsson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Sj\u00f6berg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Stenberg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2008,5,8]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1384.003"},{"key":"e_1_2_5_3_2","unstructured":"CommitteeTADC.Progress in Autoimmune Disease Research: A Report to Congress. 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