Interferon-β induces transient systemic IP-10/CXCL10 chemokine release in patients with multiple sclerosis

被引：41

作者：

Buttmann, M ^{[1
]}

Merzyn, C ^{[1
]}

Rieckmann, P ^{[1
]}

机构：

[1] Univ Wurzburg, Dept Neurol, Clin Res Unit Multiple Sclerosis & Neuroimmunol, D-97080 Wurzburg, Germany

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2004年 / 156卷 / 1-2期

关键词：

CXC chemokine IP-10; monocyte chemoattractant protein-1; interleukin-6; adverse effects;

D O I：

10.1016/j.jneuroim.2004.07.016

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Reduction of chemokine expression induced by human recombinant Interferon (IFN)-beta is thought to be a therapeutic mechanism of its action in the treatment of multiple sclerosis (MS). In vitro, IFN-beta can induce chemokine expression. Here we show that a single injection of IFN-beta induced a transient strong increase of IP-10/CXCL10 and a weak elevation of MCP-1/CCL2 plasma levels in MS patients on continuing treatment with IFN-beta. IP-10/CXCL10 bursts, which were not observed in glatiramer acetate (GA)-treated patients, correlated with occurrence of flu-like symptoms. Systemic IP-10/CXCL10 release induced by IFN-beta may influence its therapeutic effect-either negatively or positively. (C) 2004 Elsevier B.V. All rights reserved.

引用

页码：195 / 203

页数：9

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