Interleukin-27 suppresses experimental autoimmune encephalomyelitis during bone marrow stromal cell treatment

被引:42
|
作者
Wang, Jinghua [1 ]
Wang, Guangyou [1 ]
Sun, Bo [1 ]
Li, Hulun [1 ]
Mu, Lih [1 ]
Wang, Qi [1 ]
Li, Guozhong [2 ]
Shi, Lijun [3 ]
Jin, Lianhong [1 ]
Kostulas, Nikolaos [4 ]
机构
[1] Harbin Med Coll, Dept Neurobiol, Heilongjiang 150081, Peoples R China
[2] Harbin Med Coll, Affiliated Clin Coll 1, Dept Neurol, Heilongjiang 150081, Peoples R China
[3] Harbin Med Coll, Affiliated Clin Coll 1, Dept Gastroenterol, Heilongjiang 150081, Peoples R China
[4] Huddinge Univ Hosp, Dept Neurol, S-14186 Huddinge, Sweden
关键词
experimental autoimmune encephalomyelitis; bone marrow stromal cells; interleukin-17; interleukin-27; immunoregulation;
D O I
10.1016/j.jaut.2007.10.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Interleukin (IL)-17 is a key inflammatory cytokine in autoimmune disease and may play an important role in the development of experimental autoimmune encephalomyelitis (EAE). In this study, we observed decreased IL-17 and increased IL-27 in EAE rats treated with bone marrow stromal cells (BMSCs). Neutralization of IL-27 resulted in recovery of the BMSCs effect. Adoptive transfer induction of EAE was poor by BMSC-stimulated MNCs, but could be induced by MNCs stimulated by BMSCs under blockade of IL-27 signaling. These results demonstrate that BMSCs may suppress the development of EAE, possibly via secretion of IL-27, which can inhibit IL-17 production or Th17 cell generation. (C) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:222 / 229
页数:8
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