Aringer M, Smolen J S
Department of Rheumatology, Medical University of Vienna, Vienna, Austria.
Lupus. 2004;13(5):344-7. doi: 10.1191/0961203303lu1024oa.
Systemic lupus erythematosus (SLE) is an autoantibody and immune complex mediated disease. However, it is the ensuing inflammatory process that leads to irreversible organ damage. In fact several murine models of SLE suggest that this inflammatory organ damage can be prevented even in the presence of autoantibodies. Given data from experimental models as well as from patients, proinflammatory cytokines including tumour necrosis factor (TNF) alpha apparently play a significant role in the inflammatory process, but may have immunoregulatory functions at the same time. Therefore, anti-TNF alpha therapy may constitute an interesting candidate approach for treating SLE inflammatory organ disease, but potentially at the cost of increased autoantibody formation. Clinical trials will be required to answer whether TNF alpha blockade fulfils this hope with an acceptable safety profile. Interferon (IFN)-gamma, interleukin (IL)-18, IL-6 and possibly IL-1 are increased in SLE and likewise involved in the inflammatory process. Specific therapeutic agents for blocking these cytokines should be available in the near future.
系统性红斑狼疮（SLE）是一种由自身抗体和免疫复合物介导的疾病。然而，随后发生的炎症过程才会导致不可逆的器官损伤。事实上，几种SLE小鼠模型表明，即使存在自身抗体，这种炎症性器官损伤也可以预防。根据实验模型以及患者的数据，包括肿瘤坏死因子（TNF）α在内的促炎细胞因子显然在炎症过程中发挥重要作用，但同时可能具有免疫调节功能。因此，抗TNFα疗法可能是治疗SLE炎症性器官疾病的一种有趣的候选方法，但可能会以自身抗体形成增加为代价。需要进行临床试验来回答TNFα阻断是否能以可接受的安全性实现这一希望。干扰素（IFN）-γ、白细胞介素（IL）-18、IL-6以及可能的IL-1在SLE中升高，同样参与炎症过程。用于阻断这些细胞因子的特异性治疗药物在不久的将来应该会出现。
