干扰素β-1b调节复发缓解型多发性硬化症中单核细胞趋化蛋白-1的表达和产生。

Interferon beta-1b modulates MCP-1 expression and production in relapsing-remitting multiple sclerosis.

作者信息

Iarlori Carla, Reale Marcella, De Luca Giovanna, Di Iorio Angelo, Feliciani Claudio, Tulli Antonio, Conti Pio, Gambi Domenico, Lugaresi Alessandra

机构信息

Department of Oncology and Neuroscience, Neuroimmunology Unit, University "G. d'Annunzio", Via dei Vestini, I-66013, Chieti, Italy.

出版信息

J Neuroimmunol. 2002 Feb;123(1-2):170-9. doi: 10.1016/s0165-5728(01)00487-8.

DOI:10.1016/s0165-5728(01)00487-8

PMID:11880161

Abstract

Monocyte 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 MS 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.

摘要

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，在未刺激（PHA(-)）和PHA刺激（PHA(+)）的外周血单个核细胞（PBMC）中，稳定期未经治疗的MS患者的MCP-1和TNFα水平较高。在PHA(-)培养的复发患者和PHA(+)培养的稳定患者中，干扰素γ（IFNγ）水平较高。慢性IFNβ-1b治疗可下调TNFα、IFNγ和MCP-1的产生，但复发患者的TNFα除外。体外实验中，IFNβ-1b可增加所有患者的MCP-1、TNFα和IFNγ的自发产生。多变量分析表明，MCP-1的产生取决于临床状态，而非TNFα和IFNγ的产生。逻辑回归分析显示，治疗可显著改变MCP-1的产生。需要进一步研究以阐明MCP-1在MS中的作用。