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.
引用
收藏
页码:4375 / 4381
页数:7
相关论文
共 36 条
  • [1] ANDREWS DM, 1998, ANTIGEN T CELL RECEP, P373
  • [2] Interferon gamma production by natural killer (NK) cells and NK1.1(+) T cells upon NKR-P1 cross-linking
    Arase, H
    Arase, N
    Saito, T
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (05) : 2391 - 2396
  • [3] Association between alpha beta TCR(+)CD4(-)CD8(-) T-cell deficiency and IDDM in NOD/Lt mice
    Baxter, AG
    Kinder, SJ
    Hammond, KJL
    Scollay, R
    Godfrey, DI
    [J]. DIABETES, 1997, 46 (04) : 572 - 582
  • [4] Mouse CD1-specific NK1 T cells: Development, specificity, and function
    Bendelac, A
    Rivera, MN
    Park, SH
    Roark, JH
    [J]. ANNUAL REVIEW OF IMMUNOLOGY, 1997, 15 : 535 - 562
  • [5] BIX M, 1995, J IMMUNOL, V155, P1020
  • [6] CD1d-mediated recognition of an α-galactosylceramide by natural killer T cells is highly conserved through mammalian evolution
    Brossay, L
    Chioda, M
    Burdin, N
    Koezuka, Y
    Casorati, G
    Dellabona, P
    Kronenberg, M
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 188 (08) : 1521 - 1528
  • [7] Chen HJ, 1997, J IMMUNOL, V159, P2240
  • [8] CORNBLATH DR, 1991, NEUROLOGY, V41, P617
  • [9] AN INVARIANT V-ALPHA-24-J-ALPHA-Q/V-BETA-11 T-CELL RECEPTOR IS EXPRESSED IN ALL INDIVIDUALS BY CLONALLY EXPANDED CD4-8- T-CELLS
    DELLABONA, P
    PADOVAN, E
    CASORATI, G
    BROCKHAUS, M
    LANZAVECCHIA, A
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 180 (03) : 1171 - 1176
  • [10] Dyck PJ, 1993, PERIPHERAL NEUROPATH