IL-10 is essential for disease protection following intranasal peptide administration in the C57BL/6 model of EAE

被引:68
作者
O'Neill, Emma J. [1 ]
Day, Michael J.
Wraith, David C.
机构
[1] Coll Life Sci, Sch Agr Food Sci & Vet Med, Dublin 4, Ireland
[2] Univ Bristol, Dept Vet Clin Sci, Dept Vet Pathol Infect & Immun, Bristol BS40 5DU, Avon, England
[3] Univ Bristol, Sch Med, Dept Cellular & Mol Med, Bristol BS8 1TD, Avon, England
基金
英国惠康基金;
关键词
experimental autoimmune encephalomyelitis; histopathology; myelin oligodendrocyte glycoprotein (MOG); tolerance induction;
D O I
10.1016/j.jneuroim.2006.05.030
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We have shown previously that intranasal administration of encephalitogenic peptides in soluble form to H-2(u) and H-2(s) mice affords protection from experimental autoimmune encephalomyelitis (EAE). Here we demonstrate that this method of disease protection can be induced in C57BL/6 mice by administration of the soluble peptide 35-55 from myelin oligodendrocyte glycoprotein. This protective effect was demonstrated by the evaluation of both clinical EAE scores and central nervous system histopathology; the latter showing minimal inflammatory infiltrates in treated mice. The employment of an IL-10(-/-) congenic strain allowed an appraisal of the involvement of IL-10 in this process. The lack of disease protection in these mice clearly demonstrates the non-redundant role of IL-10 in this process. (c) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 8
页数:8
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