共 30 条
T-CELL RECEPTOR V-GENE USAGE OF ISLET BETA-CELL REACTIVE T-CELLS IS NOT RESTRICTED IN NONOBESE DIABETIC MICE
被引:149
作者:

NAKANO, N
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机构: OSAKA UNIV,INST MOLEC & CELLULAR BIOL,DIV IMMUNOL,1-3 YAMADA-OKA,SUITA,OSAKA 565,JAPAN

KIKUTANI, H
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机构: OSAKA UNIV,INST MOLEC & CELLULAR BIOL,DIV IMMUNOL,1-3 YAMADA-OKA,SUITA,OSAKA 565,JAPAN

NISHIMOTO, H
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机构: OSAKA UNIV,INST MOLEC & CELLULAR BIOL,DIV IMMUNOL,1-3 YAMADA-OKA,SUITA,OSAKA 565,JAPAN

KISHIMOTO, T
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机构: OSAKA UNIV,INST MOLEC & CELLULAR BIOL,DIV IMMUNOL,1-3 YAMADA-OKA,SUITA,OSAKA 565,JAPAN
机构:
[1] OSAKA UNIV,INST MOLEC & CELLULAR BIOL,DIV IMMUNOL,1-3 YAMADA-OKA,SUITA,OSAKA 565,JAPAN
[2] SHIONOGI & CO LTD,SHIONOGI RES LAB,OSAKA 553,JAPAN
关键词:
D O I:
10.1084/jem.173.5.1091
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Five islet-reactive T cell clones were established from islet-infiltrating T cells of non-obese diabetic (NOD) mice. All clones expressed CD4, but not CD8, and responded to islet cells from various strains of mice in the context of I-A(NOD). They could induce insulitis when transferred into disease-resistant I-E+ transgenic NOD mice. The T cell receptor (TCR) sequences utilized by the clones were determined. Their usage of TCR V and J segments was not restricted but was rather diverse. One of the clones utilized V-beta-16. The expression of V-beta-16 was significantly reduced in I-E+ transgenic NOD, suggesting the possibility that the islet-reactive T cell clone expressing V-beta-16 may be deleted or inactivated by I-E molecules. This clone might be one of the candidates that triggers insulitis.
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页码:1091 / 1097
页数:7
相关论文
共 30 条
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