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To explore the potential role of CD47<\/jats:styled-content> in activation of autoreactive T and B cells and the production of autoantibodies in autoimmune disease, especially systemic lupus erythematosus (SLE<\/jats:styled-content>), we have generated CD47<\/jats:styled-content> knockout Faslpr<\/jats:sup><\/jats:italic> (CD47<\/jats:styled-content>\u2212\/\u2212<\/jats:sup>\u2212Faslpr<\/jats:sup><\/jats:italic>) mice and examined histopathological changes in the kidneys, cumulative survival rates, proteinuria, extent of splenomegaly and autoantibodies, serum chemistry and immunological parameters. In comparison with Faslpr<\/jats:sup><\/jats:italic> mice, CD47<\/jats:styled-content>\u2212\/\u2212<\/jats:sup>\u2212Faslpr<\/jats:sup><\/jats:italic> mice exhibit a prolonged lifespan and delayed autoimmune nephritis, including glomerular cell proliferation, basement membrane thickening, acute tubular atrophy and vacuolization. CD47<\/jats:styled-content>\u2212\/\u2212<\/jats:sup>\u2212Faslpr<\/jats:sup><\/jats:italic> mice have lower levels of proteinuria, associated with reduced deposition of complement C3<\/jats:styled-content> and C1q, and IgG<\/jats:styled-content> but not IgM<\/jats:styled-content> in the glomeruli, compared to age\u2010matched Faslpr<\/jats:sup><\/jats:italic> mice. Serum levels of antinuclear antibodies and anti\u2010double\u2010stranded DNA<\/jats:styled-content> antibodies are significantly lower in CD47<\/jats:styled-content>\u2212\/\u2212<\/jats:sup>\u2212Faslpr<\/jats:sup><\/jats:italic> than in Faslpr<\/jats:sup><\/jats:italic> mice. CD47<\/jats:styled-content>\u2212\/\u2212<\/jats:sup>\u2013Faslpr<\/jats:sup><\/jats:italic> mice also display less pronounced splenomegaly than Faslpr<\/jats:sup><\/jats:italic> mice. The mechanistic studies further suggest that CD47<\/jats:styled-content> deficiency impairs the antigenic challenge\u2010induced production of IgG<\/jats:styled-content> but not IgM<\/jats:styled-content>, and that this effect is associated with reduction of T follicular cells and impairment of germinal centre development in lymphoid tissues. In conclusion, our results demonstrate that CD47<\/jats:styled-content> deficiency ameliorates lupus nephritis in Faslpr<\/jats:sup><\/jats:italic> mice via suppression of IgG<\/jats:styled-content> autoantibody production. Copyright \u00a9 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.4574","type":"journal-article","created":{"date-parts":[[2015,6,19]],"date-time":"2015-06-19T19:47:51Z","timestamp":1434743271000},"page":"285-295","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["CD47 deficiency ameliorates autoimmune nephritis in Faslpr<\/sup><\/i> mice by suppressing IgG autoantibody production"],"prefix":"10.1002","volume":"237","author":[{"given":"Lei","family":"Shi","sequence":"first","affiliation":[{"name":"State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Centre for MicroRNA Biology and Biotechnology Nanjing University School of Life Sciences Peoples Republic of China"},{"name":"Center for Diagnostics and Therapeutics, Center for Inflammation, Immunity and Infection, Department of Biology Georgia State University Atlanta GA 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