IFN-β1a and IFN-β1b have different patterns of influence on cytokines
IFN-β1a and IFN-β1b have different patterns of influence on cytokines
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DOI：
10.1016/j.clineuro.2004.02.010
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发表时间：
2004-06-01
影响因子：
1.9
通讯作者：
Ihan, A
中科院分区：
文献类型：
--
作者：
Sega, S;Wraber, B;Ihan, A
多发性硬化症的特点是Th1细胞产生的促炎细胞因子水平升高，Th2细胞产生的抗炎细胞因子水平降低。干扰素-β治疗将免疫应答从Th1模式转变为Th2模式，从而增强IL-4、IL-10等抗炎Th2细胞因子的产生，并减少LFN-γ等促炎症Th1细胞因子的产生。为了确定哪一种干扰素-β具有更强的免疫调节作用，我们比较了12例复发-缓解期MS患者接受干扰素-β1b治疗的IL-4、IL-10和干扰素-γ水平，并与10例接受干扰素-β1a治疗的患者(Avonex((R)进行了比较。在治疗前和治疗中的病程、复发次数以及治疗2年后的EDSS评分方面，差异均无统计学意义。治疗1年后，倍他乐组(R)干扰素-γ水平显著降低，而雅芳(R)组IL-4、IL-10水平显著升高。似乎干扰素-β1b对Th1和Th2细胞因子均有下调作用，而干扰素-β1a则导致细胞因子谱向Th2表型转变。这两种干扰素对MS的细胞因子模式有不同的影响：干扰素-β1a促进抗炎细胞因子IL-4和IL-10的产生，而干扰素-β1b减少促炎细胞因子干扰素-γ的产生。(C)2004爱思唯尔B.V.保留所有权利。
Multiple sclerosis is characterized by elevated levels of proinflammatory cytokines produced by Th1 cells and decreased levels of anti-inflammatory cytokines produced by Th2 cells. IFN-beta treatment shifts the immune response from the Th1 to Th2 pattern, thus enhancing the production of anti-inflammatory Th2 cytokines such as IL-4, IL-10, and decreasing the production of proinflammatory Th1 cytokines such as LFN-gamma. To determine which IFN-beta has the stronger immunomodulatory effect we compared the levels of IL-4, IL-10, and IFN-gamma of 12 relapsing-remiting MS patients treated with IFN-beta1b (Betaferon((R))) with those of 10 patients treated with IFN-beta1a (Avonex((R))). There were no statistically significant differences in duration of disease, number of relapses before and during treatment, and in EDSS after 2 years of treatment. After 1 year of treatment the concentration of IFN-gamma was significantly lower in the Betaferon((R)) group, and concentrations of IL-4 and IL-10 were significantly higher in the Avonex((R)) group. It appears that IFN-beta1b has a downregulatory effect on both Th1 and Th2 cytokines, while IFN-beta1a causes a shift of the cytokine profile toward the Th2 phenotype. These two IFN have different influences on the pattern of cytokines in MS: IFN-beta1a enhances the production of anti-inflammatory cytokines IL-4 and IL-10 and IFN-beta1b decreases the production of the proinflammatory cytokine IFN-gamma. (C) 2004 Elsevier B.V. All rights reserved.