Of the multiple murine models of autoimmunity, the three most closely resembling human systemic lupus erythematosus (SLE) are the MRL/lpr, New Zealand Black/White F(1), and male BXSB. Although these strains share many disease characteristics, no common cellular defect has previously been found in prediseased mice from all these strains. We show in this study that macrophages from prediseased mice of all three SLE-prone strains, as well as macrophages from mice whose genomes contribute to the development of SLE (MRL/+, New Zealand White, New Zealand Black, female BXSB, and LG/J), have an identical and profound defect in cytokine expression that is triggered by apoptotic cells. Strikingly, none of 13 nonautoimmune strains tested exhibited this defect. Given that apoptotic Ags have been increasingly recognized as the target of autoantibodies, a defect in cytokine expression that is triggered by apoptotic cells has broad potential to upset the balance between tolerance and immunity.

译文

在自身免疫的多种鼠模型中,最类似于人类系统性红斑狼疮 (SLE) 的三种是MRL/lpr,新西兰黑/白F(1) 和雄性BXSB。尽管这些菌株具有许多疾病特征,但以前在所有这些菌株的患病小鼠中未发现常见的细胞缺陷。我们在这项研究中表明,来自所有三种SLE易患菌株的患病小鼠的巨噬细胞,以及来自其基因组有助于SLE发展的小鼠的巨噬细胞 (MRL/,新西兰白人,新西兰黑人,雌性BXSB和LG/J),凋亡细胞触发的细胞因子表达具有相同且深刻的缺陷。令人惊讶的是,测试的13种非自身免疫菌株均未显示出这种缺陷。鉴于凋亡Ags已被越来越多地视为自身抗体的靶标,凋亡细胞触发的细胞因子表达缺陷具有破坏耐受性和免疫力之间平衡的广泛潜力。

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