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Galectin 9 (Gal\u20109, <jats:italic>Lgals9<\/jats:italic>) is a \u03b2\u2010galactoside\u2013binding lectin that has been used for clinical application in autoimmune diseases, since recombinant Gal\u20109, as a ligand for T cell immunoglobulin and mucin domain\u2013containing protein 3 (<jats:styled-content style=\"fixed-case\">TIM<\/jats:styled-content>\u20103), induces apoptosis of activated <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4+<jats:styled-content style=\"fixed-case\">TIM<\/jats:styled-content>\u20103+ Th1 cells. This study was undertaken to investigate whether deficiency of <jats:italic>Lgals9<\/jats:italic> has beneficial or deleterious effects on lupus in a murine model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Gal\u20109<jats:sup>+\/+<\/jats:sup> and Gal\u20109<jats:sup>\u2212\/\u2212<\/jats:sup> female <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c mice were injected with pristane, and the severity of arthritis, proteinuria, and levels of autoantibody production were assessed at several time points immediately following injection. At 7 months after pristane injection, renal pathologic features, the severity of joint inflammation, and formation of lipogranulomas were evaluated. Subsets of inflammatory cells in the spleen and peritoneal lavage were characterized, and expression levels of cytokines from peritoneal macrophages were analyzed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Lgals9<\/jats:italic> deficiency protected against the development of immune complex glomerulonephritis, arthritis, and peritoneal lipogranuloma formation in BALB\/c mice in this murine model of pristane\u2010induced lupus. The populations of T cell subsets and B cells in the spleen and peritoneum were not altered by <jats:italic>Lgals9<\/jats:italic> deficiency in pristane\u2010injected <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c mice. Furthermore, <jats:italic>Lgals9<\/jats:italic> deficiency protected against pristane\u2010induced lupus without altering the Toll\u2010like receptor 7\u2013type I interferon pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Gal\u20109 is required for the induction and development of lupus nephritis and arthritis in this murine model of <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>. The results of the current investigation provide a potential new strategy in which antagonism of Gal\u20109 may be beneficial for the treatment of nephritis and arthritis in patients with <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content> through targeting of activated macrophages.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.40467","type":"journal-article","created":{"date-parts":[[2018,2,26]],"date-time":"2018-02-26T15:22:36Z","timestamp":1519658556000},"page":"1089-1101","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Role of <i>Lgals9<\/i> Deficiency in Attenuating Nephritis and Arthritis in <scp>BALB<\/scp>\/c Mice in a Pristane\u2010Induced Lupus Model"],"prefix":"10.1002","volume":"70","author":[{"given":"Sonia","family":"Zeggar","sequence":"first","affiliation":[{"name":"Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama 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