{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T08:15:17Z","timestamp":1768896917817,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,1,25]],"date-time":"2013-01-25T00:00:00Z","timestamp":1359072000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2013,3]]},"abstract":"We previously established an I<\/jats:styled-content>gG F<\/jats:styled-content>c receptor IIB<\/jats:styled-content> (F<\/jats:styled-content>c\u03b3RIIB<\/jats:styled-content>)\u2010deficient C<\/jats:styled-content>57BL<\/jats:styled-content>\/6 (B<\/jats:styled-content>6)\u2010congenic mouse strain (KO<\/jats:styled-content>1), which spontaneously develops rheumatoid arthritis (RA<\/jats:styled-content>), but not systemic lupus erythematosus (SLE<\/jats:styled-content>). Here, we show that when Y<\/jats:styled-content> chromosome\u2010linked autoimmune acceleration (Y<\/jats:styled-content>aa<\/jats:italic>) mutation was introduced in KO<\/jats:styled-content>1 strain (KO<\/jats:styled-content>1.Y<\/jats:styled-content>aa<\/jats:italic>), the majority of KO<\/jats:styled-content>1.Y<\/jats:styled-content>aa<\/jats:italic> mice did not develop RA<\/jats:styled-content>, but instead did develop SLE<\/jats:styled-content>. This phenotype conversion did not depend on autoantibody specificity, since KO<\/jats:styled-content>1.Y<\/jats:styled-content>aa<\/jats:italic> mice, compared with KO<\/jats:styled-content>1, showed a marked increase in serum levels of both lupus\u2010related and RA<\/jats:styled-content>\u2010related autoantibodies. The increase in frequencies of CD<\/jats:styled-content>69+<\/jats:sup> activated B<\/jats:styled-content> cells and T<\/jats:styled-content> cells, and the spontaneous splenic GC<\/jats:styled-content> formation with T<\/jats:styled-content> follicular helper cell generation were manifest early in life of KO<\/jats:styled-content>1.Y<\/jats:styled-content>aa<\/jats:italic>, but not KO<\/jats:styled-content>1 and B<\/jats:styled-content>6.Y<\/jats:styled-content>aa<\/jats:italic>, mice. Activated CD<\/jats:styled-content>4+<\/jats:sup> T<\/jats:styled-content> cells from KO<\/jats:styled-content>1.Y<\/jats:styled-content>aa<\/jats:italic> mice showed upregulated production of IL<\/jats:styled-content>\u201021 and IL<\/jats:styled-content>\u201010, compared with the finding in KO<\/jats:styled-content>1 mice, indicating the possibility that this aberrant cytokine milieu relates to the disease phenotype conversion. Thus, our model is useful to clarify the shared and the disease\u2010specific mechanisms underlying the clinically distinct systemic autoimmune diseases RA<\/jats:styled-content> and SLE<\/jats:styled-content>.<\/jats:p>","DOI":"10.1002\/eji.201243057","type":"journal-article","created":{"date-parts":[[2012,12,26]],"date-time":"2012-12-26T14:16:57Z","timestamp":1356531417000},"page":"770-778","source":"Crossref","is-referenced-by-count":10,"title":["Phenotype conversion from rheumatoid arthritis to systemic lupus erythematosus by introduction of Y<\/scp>aa<\/i> mutation into F<\/scp>c\u03b3RIIB<\/scp>\u2010deficient C<\/scp>57BL<\/scp>\/6 mice"],"prefix":"10.1002","volume":"43","author":[{"given":"Shinya","family":"Kawano","sequence":"first","affiliation":[{"name":"Department of Internal Medicine Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qingshun","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Pathology Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hirofumi","family":"Amano","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshiyuki","family":"Kaneko","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Keiko","family":"Nishikawa","sequence":"additional","affiliation":[{"name":"Department of Pathology Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiromichi","family":"Tsurui","sequence":"additional","affiliation":[{"name":"Department of Pathology Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norihiro","family":"Tada","sequence":"additional","affiliation":[{"name":"Atopy Research Center Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroyuki","family":"Nishimura","sequence":"additional","affiliation":[{"name":"Toin Human Science and Technology Center Department of Biomedical Engineering Toin University of Yokohama Yokohama Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshiyuki","family":"Takai","sequence":"additional","affiliation":[{"name":"Department of Experimental Immunology and CREST of JST Institute of Development Aging and Cancer Tohoku University Sendai Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshikazu","family":"Shirai","sequence":"additional","affiliation":[{"name":"Department of Pathology Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshinari","family":"Takasaki","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sachiko","family":"Hirose","sequence":"additional","affiliation":[{"name":"Department of Pathology Juntendo University School of Medicine Tokyo Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2013,1,25]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.09.040191.002325"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s002510050641"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/11.10.1685"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.8.4340"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.3.1646"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.30485"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.4.2352"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1101194"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0603912103"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2004.10.009"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830240531"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.5.2293"},{"key":"e_1_2_7_14_1","doi-asserted-by":"crossref","first-page":"1633","DOI":"10.1001\/archinte.1988.00380070117028","article-title":"\u2018Rhupus\u2019 syndrome","volume":"148","author":"Panush R. 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