Key result
IL-18 deletion reduces renal pathogenesis in lupus mice without altering survival or lymphadenopathy.
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The role of IL-18 in the pathogenesis of systemic lupus erythematosus is still not definitively solved. In this study, we generated MRLlpr mice, which develop a disease resembling systemic lupus erythematosus, genetically devoid of IL-18 expression. These mice in comparison to IL-18-competent MRLlpr mice show reduced signs of renal pathogenesis, while other parameters such as mean survival time, lymphadenopathy, constitutive interferon-γ production, and frequency of CD3+B220+ abnormal T cells were without differences. We conclude that in the systemic lupus erythematosus syndrom IL-18 is involved specifically in the renal pathogenesis.
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Schirmer et al. (2015) studied Systemic lupus erythematosus (MRLlpr mouse model). Genetic deletion of IL-18 expression vs. IL-18-competent MRLlpr mice was evaluated on Signs of renal pathogenesis (spontaneous kidney failure). Genetic deletion of IL-18 expression in MRLlpr mice reduced signs of renal pathogenesis without affecting survival, lymphadenopathy, or constitutive interferon-gamma production.
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