{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T20:42:33Z","timestamp":1770151353304,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2014,7,28]],"date-time":"2014-07-28T00:00:00Z","timestamp":1406505600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["1025143"],"award-info":[{"award-number":["1025143"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>The BXSB.<jats:italic>Yaa<\/jats:italic> mouse strain is a model of systemic lupus erythematosus that is dependent on duplication of the Toll\u2010like receptor 7 gene. The objective of this study was to systematically describe the amplified autoimmune phenotype observed when the soluble plasma protein \u03b2<jats:sub>2<\/jats:sub>\u2010glycoprotein I (\u03b2<jats:sub>2<\/jats:sub>GPI) gene was deleted in male BXSB.<jats:italic>Yaa<\/jats:italic> mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We generated BXSB.<jats:italic>Yaa<\/jats:italic> and NZW mouse strains in which the \u03b2<jats:sub>2<\/jats:sub>GPI gene had been knocked out by backcrossing the wild\u2010type strains with C57BL\/6 \u03b2<jats:sub>2<\/jats:sub>GPI<jats:sup>\u2212\/\u2212<\/jats:sup> mice for 10 generations. Sex\u2010 and age\u2010matched mice of the various strains were housed under identical conditions and were killed at fixed time intervals. Serum and tissue specimens were collected at various time points. Lupus\u2010associated autoantibodies, inflammatory cytokines, and the type I interferon (IFN) gene signature were measured. Flow cytometric analyses of lymphocyte populations were performed. The severity of glomerulonephritis was graded by 2 independent renal histopathologists.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Male BXSB.<jats:italic>Yaa<\/jats:italic> \u03b2<jats:sub>2<\/jats:sub>GPI<jats:sup>\u2212\/\u2212<\/jats:sup> mice developed significant lymphadenopathy and splenomegaly compared with age\u2010matched controls. Male BXSB.<jats:italic>Yaa<\/jats:italic> \u03b2<jats:sub>2<\/jats:sub>GPI<jats:sup>\u2212\/\u2212<\/jats:sup> mice also had significantly higher levels of autoantibodies, increased levels of inflammatory cytokines including tumor necrosis factor \u03b1, interleukin\u20106, and BAFF, and more severe glomerulonephritis. The type I IFN gene signature in male BXSB.<jats:italic>Yaa<\/jats:italic> \u03b2<jats:sub>2<\/jats:sub>GPI<jats:sup>\u2212\/\u2212<\/jats:sup> mice was significantly higher than that in control mice. Male BXSB.<jats:italic>Yaa<\/jats:italic> \u03b2<jats:sub>2<\/jats:sub>GPI<jats:sup>\u2212\/\u2212<\/jats:sup> mice also had marked dysregulation of various B cell and T cell populations in the spleens and lymph nodes and a disturbance in apoptotic cell clearance.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Deletion of \u03b2<jats:sub>2<\/jats:sub>GPI accelerates and potentiates the autoimmune phenotype in male BXSB.<jats:italic>Yaa<\/jats:italic> mice.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.38646","type":"journal-article","created":{"date-parts":[[2014,4,1]],"date-time":"2014-04-01T14:09:46Z","timestamp":1396361386000},"page":"2270-2280","source":"Crossref","is-referenced-by-count":17,"title":["Deletion of the Antiphospholipid Syndrome Autoantigen \u03b2<sub>2<\/sub>\u2010Glycoprotein I Potentiates the Lupus Autoimmune Phenotype in a Toll\u2010like Receptor 7\u2013Mediated Murine 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