Chemokine-enhanced migration of human peripheral blood mononuclear cells is antagonized by interferon beta-1b through an effect on matrix metalloproteinase-9

被引：98
作者：
Stuve, O
Chabot, S
Jung, SS
Williams, G
Yong, VW
机构：
[1] UNIV CALGARY,DEPT ONCOL,CALGARY,AB T2N 4N1,CANADA
[2] UNIV CALGARY,DEPT CLIN NEUROSCI,CALGARY,AB T2N 4N1,CANADA
[3] MCGILL UNIV,DEPT NEUROL & NEUROSURG,MONTREAL,PQ,CANADA
来源：
JOURNAL OF NEUROIMMUNOLOGY | 1997年 / 80卷 / 1-2期
关键词：
cell trafficking; extracellular matrix; lymphocyte; multiple sclerosis;
D O I：
10.1016/S0165-5728(97)00134-3
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
The increased migration of peripheral blood mononuclear cells (PBMNCs) across a fibronectin (FN) matrix in response to the chemokines RANTES, MIP-1 alpha and MCP-1 is antagonized by interferon beta-1b (IFN beta-1b). MCP-1 treatment of PBMNCs elevates their mRNA level and secretion of a matrix degrading enzyme, matrix metalloproteinase (MMP)-9, which is abrogated by IFN beta-1b. The clinical benefits of IFN beta-1b treatment in multiple sclerosis patients may in part be a result of this drug's ability to decrease the migration of PBMNCs in spite of a chemotactic gradient. Furthermore, the elevation of MMP-9 production by PBMMCs may be an important mechanism of action of chemokines. (C) 1997 Elsevier Science B.V.
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收藏
页码：38 / 46
页数：9
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