Differential expression of NK T cell Vα24JαQ invariant TCR chain in the lesions of multiple sclerosis and chronic inflammatory demyelinating polyneuropathy

被引:216
作者
Illés, Z
Kondo, T
Newcombe, J
Oka, N
Tabira, T
Yamamura, T
机构
[1] Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Immunol, Kodaira, Tokyo 1878502, Japan
[2] Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Demyelinating Dis & Aging, Kodaira, Tokyo 1878502, Japan
[3] Inst Neurol, London WC1N 3BG, England
[4] Kyoto Univ, Fac Med, Dept Neurol, Kyoto 606, Japan
关键词
D O I
10.4049/jimmunol.164.8.4375
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Human V alpha 24(+) NK T cells are a unique subset of lymphocytes expressing the V alpha 24J alpha Q invariant TCR chain. Because they can rapidly produce large amounts of regulatory cytokines, a reduction of NK T cells may lead to the development of certain autoimmune diseases. Using a single-strand conformation polymorphism method, we demonstrate that a great reduction of V alpha 24J alpha Q NK T cells in the peripheral blood is an immunological hallmark of multiple sclerosis, whereas it is not appreciable in other autoimmune/inflammatory diseases such as chronic inflammatory demyelinating polyneuropathy, The chronic inflammatory demyelinating polyneuropathy lesions were often found to be infiltrated with V alpha 24J alpha Q NK T cells, but multiple sclerosis lesions only rarely expressed the V alpha 24J alpha Q TCR. It is therefore possible that the extent of NK T cell alteration may be a critical factor which would define the clinical and pathological features of autoimmune disease. Although the mechanism underlying the NK T cell deletion remains largely unclear, a remarkable contrast between the CNS and peripheral nervous system diseases allows us to speculate a role of tissue-specific elements such as the level of CD1d expression or differences in the CD1d-bound glycolipid.
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收藏
页码:4375 / 4381
页数:7
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