Downregulation of IL-17 and IL-6 in the central nervous system by glatiramer acetate in experimental autoimmune encephalomyelitis

被引：48

作者：

Begum-Haque, Sakhina ^{[1
,2
]}

Sharma, Alok ^{[1
,2
]}

Kasper, Isaac R. ^{[1
,2
]}

Foureau, David M. ^{[1
,2
]}

Mielcarz, Daniel W. ^{[1
,2
]}

Haque, Azizul ^{[1
,2
,3
]}

Kasper, Lloyd H. ^{[1
,2
]}

机构：

[1] Dartmouth Med Sch, Dept Med, Lebanon, NH 03756 USA

[2] Dartmouth Coll, Multiple Sclerosis Ctr, Hanover, NH 03755 USA

[3] UPRES, Chercheur CNRS, Fac Med Lille, EA 3610, F-59037 Lille, France

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2008年 / 204卷 / 1-2期

关键词：

Animals-rodent; Diseases-EAE/MS; Molecules-cytokine receptors; Transcription factors;

D O I：

10.1016/j.jneuroim.2008.07.018

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

T helper 17 (Th17) cells are pivotal in the immune pathogenesis of EAE. Glatiramer acetate (GA) can enhance T-reg FOXp3 expression. We demonstrate that CA downregulates the expression of both IL-17 and IL-6 in two different EAE models. Increased mRNA expression in CNS for ROR gamma t, IL-17, IL-12/ IL-23, IL-6, TNF-alpha, STAT4 and Th1 cytokines were significantly reduced by CA with a concomitant rise in SMAD3. The increased expression of TNF-alpha, IL-6, and IL-17 in CNS of CD25(+) depleted animals was suppressed by CA treatment. This study demonstrates that both Th1 polarization and Th17 expression are modulated by GA. (C) 2008 Elsevier B.V. All rights reserved.

引用

页码：58 / 65

页数：8

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