Induction of low dose oral tolerance in IL-10 deficient mice with experimental autoimmune encephalomyelitis

被引:14
作者
Gonnella, PA
Waldner, HP
Kodali, D
Weiner, HL
机构
[1] Harvard Univ, Sch Med, Boston, MA 02115 USA
[2] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Cambridge, MA 02138 USA
关键词
autoimmunity; cytokines; EAE; IL-10; tolerance;
D O I
10.1016/j.jaut.2004.08.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
IL-10 has been shown to be an important anti-inflammatory mediator that has both down-regulatory and immunomodulatory effects. Utilizing IL-10(-/-) mice we demonstrate the induction of low dose oral tolerance characterized by the up-regulation of TGF-beta and IL-4 and the suppression of Ag specific proliferation with little suppression of INF-gamma. More severe EAE was found in IL-10(-/-) mice than in wild type controls, however, feeding resulted in amelioration of disease severity in both groups. Orally tolerized IL-10(-/-) mice had greater disease severity compared to orally tolerized wild type mice. IL-4 Was present in the GALT of IL-10(-/-) mice and up-regulation of TGF-beta was detected in the lamina propria of fed mice. These results demonstrate that IL-10 is not required for the induction of low dose oral tolerance but is required for the tegulation of INF-gamma which affects severity of disease in tolerized mice. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:193 / 200
页数:8
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