解析驱动狼疮发病机制的免疫细胞混乱。
Dissecting the immune cell mayhem that drives lupus pathogenesis.
机构信息
Section of Rheumatology, Department of Internal Medicine, and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
出版信息
Sci Transl Med. 2011 Mar 9;3(73):73ps9. doi: 10.1126/scitranslmed.3002138.
Abstract
The autoimmune disease systemic lupus erythematosus (SLE) results from an inability of the immune system to discriminate between certain self-antigens and foreign ones. The most common treatment of SLE involves the use of immunosuppressive drugs to reduce inflammation, but these therapies have serious side effects. Three recent papers in Science Translational Medicine redirect focus on neutrophils, platelets, and interferon-α in the pathogenesis of SLE and reinforce the notion that researchers should seek to discover and devise combination therapies that target these processes.
摘要
自身免疫性疾病系统性红斑狼疮 (SLE) 是由于免疫系统无法区分某些自身抗原和外来抗原而导致的。SLE 的最常见治疗方法涉及使用免疫抑制剂来减轻炎症，但这些疗法有严重的副作用。最近在《科学转化医学》上的三篇论文重新关注中性粒细胞、血小板和干扰素-α 在 SLE 发病机制中的作用，并强化了这样一种观点，即研究人员应该寻求发现和设计针对这些过程的联合疗法。
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本文引用的文献
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Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus.网织中性粒细胞是小儿全身性红斑狼疮中 I 型 IFN 产生的主要诱导剂。
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Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps.中性粒细胞弹性蛋白酶和髓过氧化物酶调节中性粒细胞细胞外陷阱的形成。
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