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Mechanisms of disease: macrophage migration inhibitory factor in SLE, RA and atherosclerosis.

机译:疾病机理:SLE,RA和动脉粥样硬化中的巨噬细胞迁移抑制因子。

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The past decade has seen the emergence of two new paradigms in inflammatory disease: first, cardiovascular complications of atherosclerosis are markedly increased in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE); and second, inflammatory mechanisms are important in the pathogenesis of atherosclerosis. These concurrent developments have lead to the concept that inflammatory mediators operative in RA and SLE might be causal in the accelerated atherosclerosis observed, a concept supported by clinical studies showing that this acceleration is not fully explained by traditional vascular risk factors. Separate lines of evidence implicate the cytokine macrophage migration inhibitory factor (MIF) in RA, SLE, and atherosclerosis. Several reports have revealed definitive in vivo evidence of the activity of MIF in a model of SLE, demonstrated a novel role for MIF in monocyte/macrophage recruitment, and showed that MIF regulates a key mediator of inflammatory cell activation. Together with evidence that MIF circulates in increased concentrations in patients with RA and SLE, this information suggests that in addition to contributing to each disease, MIF might contribute directly to the acceleration of atherosclerosis in RA and SLE.
机译:在过去的十年中,出现了两种新的炎性疾病范例:首先,类风湿关节炎(RA)和系统性红斑狼疮(SLE)患者的动脉粥样硬化心血管并发症明显增加;其次,炎症机制在动脉粥样硬化的发病机理中很重要。这些并发的发展导致了这样一个概念,即在RA和SLE中起作用的炎症介质可能是观察到的动脉粥样硬化加速的原因,临床研究支持这一概念,表明传统血管危险因素不能完全解释这种加速。单独的证据暗示RA,SLE和动脉粥样硬化中的细胞因子巨噬细胞迁移抑制因子(MIF)。几篇报道揭示了SLE模型中MIF活性的确切体内证据,证明了MIF在单核细胞/巨噬细胞募集中的新作用,并表明MIF调节了炎症细胞激活的关键介体。连同有证据表明MIF在RA和SLE患者中以更高的浓度循环,该信息表明MIF除了助长每种疾病外,还可能直接促进RA和SLE的动脉粥样硬化。

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