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- W1517750168 abstract "Abstract Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the production of autoantibodies and inflammatory damage in target organs. Kidney involvement affects up to 60% of lupus patients, and is responsible for significant morbidity and mortality. Previous studies using methods to reduce macrophage number have reached conflicting conclusions regarding the role of macrophages in lupus nephritis (LN). Moreover, “off target” effects occur in mice congenitally deficient in macrophages. In this study, we investigated the role of macrophages in mice receiving anti-glomerular antibodies, or nephrotoxic serum (NTS), an experimental model which closely mimics the immune complex mediated disease seen in LN. GW2580, an oral kinase inhibitor monospecific for the CSF-1 receptor, was used as a novel and highly selective method for macrophage depletion. We found that GW2580-treated NTS challenged mice did not develop the significant increases in levels of proteinuria, serum creatinine or serum urea, seen in control treated mice. Further, GW2580-treated mice were protected from the robust kidney expression of inflammatory cytokines associated with LN seen in control treated mice, including RANTES, IP-10, VCAM1, MCP-1 and IL-6. IBA-1 staining confirmed profound depletion of macrophages in glomeruli of GW2580-treated mice. Our results support an important role of macrophages in LN, and suggest targeting this cell type as a promising approach to the treatment of LN." @default.
- W1517750168 created "2016-06-24" @default.
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- W1517750168 date "2014-05-01" @default.
- W1517750168 modified "2023-10-16" @default.
- W1517750168 title "Macrophage depletion ameliorates nephritis induced by pathogenic antibodies (BA12P.111)" @default.
- W1517750168 doi "https://doi.org/10.4049/jimmunol.192.supp.176.12" @default.
- W1517750168 hasPublicationYear "2014" @default.
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