Richaud-Patin Y, Alcocer-Varela J, Llorente L
Departamento de Inmunología y Reumatología, Instituto Nacional de la Nutrición Salvador Zubirán, México, D.F.
Rev Invest Clin. 1995 Jul-Aug;47(4):267-72.
Systemic lupus erythematosus (SLE) is an autoimmune disease with a clear imbalance in the network made up of different cytokines. However this statement has been derived from studies which have focused on the analysis of some specific cytokines and few have simultaneously analyzed those cytokines that could be involved in the pathogenesis of SLE. Therefore, we decided to analyze interleukin IL-1b, IL-2, IL-4, IL-6, IL-10, tumor necrosis factor-a (TNF-a) and gamma interferon (IFN-g) gene expression in peripheral blood mononuclear cells from 17 women with SLE and 10 normal females by a coupled reverse transcriptase-polymerase chain reaction technique. High gene expression of IL-4, IL-6, IL-10 and TNF-a was found in SLE patients as compared to normal subjects. The expression of IL-1b, IL-2 and IFN-g genes was low or undetectable. The resulting high level of cytokines with strong effect on proliferation and differentiation of B lymphocytes in SLE could be responsible for the characteristic B cell hyperactivity and autoantibody production seen in SLE.
系统性红斑狼疮(SLE)是一种自身免疫性疾病,在由不同细胞因子组成的网络中存在明显失衡。然而,这一说法源于专注于某些特定细胞因子分析的研究,很少有研究同时分析那些可能参与SLE发病机制的细胞因子。因此,我们决定采用逆转录聚合酶链反应技术,分析17例SLE女性患者和10例正常女性外周血单个核细胞中白细胞介素IL-1β、IL-2、IL-4、IL-6、IL-10、肿瘤坏死因子-α(TNF-α)和γ干扰素(IFN-γ)的基因表达。与正常受试者相比,SLE患者中IL-4、IL-6、IL-10和TNF-α的基因表达较高。IL-1β、IL-2和IFN-γ基因的表达较低或无法检测到。SLE中产生的高水平细胞因子对B淋巴细胞的增殖和分化有强烈影响,可能是SLE中特征性B细胞过度活跃和自身抗体产生的原因。