Glatiramer acetate reduces Th-17 inflammation and induces regulatory T-cells in the CNS of mice with relapsing-remitting or chronic EAE

被引：62

作者：

Aharoni, Rina ^{[1
]}

Eilam, Raya ^{[1
]}

Stock, Ariel ^{[1
]}

Vainshtein, Anya ^{[1
]}

Shezen, Elias ^{[1
]}

Gal, Hilah ^{[1
]}

Friedman, Nir ^{[1
]}

Arnon, Ruth ^{[1
]}

机构：

[1] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2010年 / 225卷 / 1-2期

基金：

以色列科学基金会;

关键词：

Multiple sclerosis; Experimental autoimmune encephalomyelitis; Interleukin-17; T-regulatory cells; lmmunomodulation; Glatiramer acetate; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; MYELIN BASIC-PROTEIN; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; COPOLYMER; MECHANISMS; DISEASE; BRAIN; IL-17;

D O I：

10.1016/j.jneuroim.2010.04.022

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 aim of this study was to identify cell populations relevant to pathogenesis and repair within the injured CNS in mice that recovered from experimental autoimmune encephalomyelitis (EAE). We demonstrate that in two EAE models, with either relapsing remitting or chronic course, T-cells and resident activated microglia manifested extensive IL-17 expression, with apparent localization within regions of myelin loss. In mice treated with glatiramer acetate (GA. Copaxone (R)), even when treatment started after disease exacerbation, CNS inflammation and Th-17 occurrence were drastically reduced, with parallel elevation in T-regulatory cells, indicating the immunomodulatory therapeutic consequences of GA treatment in situ. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：100 / 111

页数：12

共 34 条

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AFZALI B, 2009, CLIN EXPT IMMUNOLOGY, P1

[2] The immunomodulator glatiramer acetate augments the expression of neurotrophic factors in brains of experimental autoimmune encephalomyelitis mice [J].