Mechanism of natural killer (NK) cell regulatory role in experimental autoimmune encephalomyelitis

被引:91
|
作者
Xu, W
Fazekas, G
Hara, H
Tabira, T
机构
[1] Natl Inst Longev Sci, Morioka, Obu 4748522, Japan
[2] Natl Ctr Neurol & Psychiat, Dept Demyelinating Dis & Aging, Tokyo 1878502, Japan
[3] Harbin Med Coll, Dept Immunol, Harbin 150086, Peoples R China
关键词
natural killer cells; experimental autoimmune encephalomyelitis; proteolipid protein; encephalitogenicity; cytotoxicity;
D O I
10.1016/j.jneuroim.2005.02.011
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 mechanism of natural killer (NK) cell regulatory role in experimental autoimmune encephalomyelitis (EAE) was studied in SJL/J mice. In vivo experiments showed that NK cell depletion by anti-NK1.1 monoclonal antibody treatment enhanced EAE in mice. To investigate the mechanism, we cultured proteolipid protein (PLP)(136-150) peptide-specific, encephalitogenic T cell lines, which were used as the NK cell target. Our results show that NK cells exert a direct cytotoxic effect on autoantigen-specific, encephalitogenic T cells. Furthermore, cytotoxicity to PLP-specific, encephalitogenic T I me cells was enhanced by using enriched NK cells as effector cells. However, the cytotoxic effect of NK cells to ovalbumin-specific T line cells and ConA-stimulated T cells could also be detected with a lesser efficiency. Our studies indicate that NK cells play a regulatory role in EAE through killing of syngeneic T cells which include myelin antigen-specific, encephalitogenic T cells, and thus ameliorate EAE. (C) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:24 / 30
页数:7
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