Interferon β-1b modulates MCP-1 expression and production in relapsing-remitting multiple sclerosis
Interferon β-1b modulates MCP-1 expression and production in relapsing-remitting multiple sclerosis
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DOI：
10.1016/s0165-5728(01)00487-8
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发表时间：
2002-02-01
影响因子：
3.3
通讯作者：
Lugaresi, A
中科院分区：
文献类型：
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作者：
Iarlori, C;Reale, M;Lugaresi, A
单核细胞趋化蛋白-1 （MCP-1）似乎参与了多发性硬化症（MS）的发病机制。我们发现在未受刺激的（PHA(-)）和受PHA刺激的（PHA(+)）外周血单个核细胞（PBMC）中，稳定的未经治疗的NIS患者的MCP-1和TNFalpha水平较高。干扰素γ (IFNgamma)在PHA（-）培养的复发患者和PHA（-）培养的稳定患者中较高。慢性ifnβ -1b治疗可下调复发患者中除TNFalpha外的TNFalpha、IFNgamma和MCP-1的产生。在体外，ifnβ -1b增加了所有患者MCP-1、TNFalpha和IFNgamma的自发产生。多变量分析表明，MCP-1的产生取决于临床状态，而不取决于TNFalpha和IFNgamma的产生。Logistic回归分析表明，处理显著改变了MCP-1的产量。需要进一步的研究来阐明MCP-1在ms中的作用(C) 2002 Elsevier Science B.V.版权所有。
lMonocyte chemoattractant protein-1 (MCP-1) seems to be involved in the pathogenesis of multiple sclerosis (MS). We found that in unstimulated (PHA(-)) and PHA-stimulated (PHA(+)) peripheral blood mononuclear cells (PBMC), MCP-1 and TNFalpha levels are higher in stable untreated NIS patients. Interferon gamma (IFNgamma) is higher in relapsing patients in PHA(-) cultures and in stable patients in PHA(-) cultures. Chronic IFNbeta-1b treatment down-regulates TNFalpha, IFNgamma and MCP-1 production except for TNFalpha in relapsing patients. IFNbeta-1b, in vitro, increases MCP-1, TNFalpha and IFNgamma spontaneous production in all patients. Multivariate analysis suggests that MCP-1 production is dependent from clinical status and not from TNFalpha and IFNgamma production. Logistic regression analysis shows that MCP-1 production is significantly modified by treatment. Further studies are needed to clarify the role of MCP-1 in MS. (C) 2002 Elsevier Science B.V. All rights reserved.