Robak E, Sysa-Jedrzejowska A, Robak T
Katedry i Kliniki Dermatologii i Wenerologii Akademii Medycznej w Lodzi.
Przegl Lek. 1996;53(8):623-6.
In systemic lupus erythematosus (SLE) is a disease characterized by B cell hyperactivity, autoantibody production and immune complex deposition in vital organs. To explain the mechanisms responsible for immune dysregulation in SLE cytokines have received increasing attention. This review has discussed a number of cytokines which appear to be involved in lupus pathogenesis. Recent studies have shown that disease activity and the main symptoms of SLE are associated with increasing serum levels of cytokines such as interleukin-(IL)-1, IL-2, IL-6, interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (THF-alpha). Constitutive expression and in vitro induction of specific cytokines are also aberrant in SLE. The presence of IL-1, IL-6 and IFN-gamma in involved kidneys suggests that they have local pathogenic effects. Moreover IFN-gamma, IL-6 and IL-1 modulate spontaneous IgG production by SLE mononuclear cells. During the next several years, the exact role of these cytokine in the pathogenesis of lupus become more fully elucidated.
系统性红斑狼疮（SLE）是一种以B细胞活性亢进、自身抗体产生以及免疫复合物在重要器官沉积为特征的疾病。为了解释SLE中免疫失调的机制，细胞因子受到了越来越多的关注。本综述讨论了一些似乎参与狼疮发病机制的细胞因子。最近的研究表明，SLE的疾病活动和主要症状与血清中白细胞介素-（IL）-1、IL-2、IL-6、干扰素-γ（IFN-γ）和肿瘤坏死因子-α（THF-α）等细胞因子水平升高有关。SLE中特定细胞因子的组成性表达和体外诱导也存在异常。受累肾脏中存在IL-1、IL-6和IFN-γ表明它们具有局部致病作用。此外，IFN-γ、IL-6和IL-1调节SLE单核细胞自发产生IgG。在接下来的几年里，这些细胞因子在狼疮发病机制中的确切作用将得到更充分的阐明。
