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TYPE-1 DIABETES-MELLITUS - AN IMBALANCE BETWEEN EFFECTOR AND REGULATORY T-CELLS
被引:9
作者:
RASHBA, EJ
[1
]
REICH, EP
[1
]
JANEWAY, CA
[1
]
SHERWIN, RS
[1
]
机构:
[1] YALE UNIV,SCH MED,DEPT INTERNAL MED,ENDOCRINOL SECT,BOX 3333,FITKIN I,NEW HAVEN,CT 06510
关键词:
AUTOIMMUNITY;
DIABETES;
NOD MOUSE;
REGULATION;
T-CELLS;
D O I:
10.1007/BF00578215
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Abundant evidence now exists that autoimmunity plays a critical role in the pathogenesis of type 1 (insulin-dependent) diabetes mellitus. The non-obese diabetic (NOD) mouse is an extensively studied animal model of this T-cell-mediated autoimmune disease. Our laboratory has focused on isolating diabetogenic T cell clones from NOD mice as a means of elucidating the pathogenesis of type 1 diabetes. This experimental approach pre-supposes that type 1 diabetes in NOD mice results from the action of islet-reactive T cells that are not present in other mouse strains; the diabetogenic T cells would therefore represent ''forbidden clones'' which exist in NOD mice as a result of a failure of clonal deletion. While the inappropriate presence of diabetogenic T cells probably plays a central role in murine diabetes, it cannot explain all aspects of the disease. Type 1 diabetes is a chronic disorder with a lengthy preclinical stage; if the diabetogenic T cells acted in an unopposed fashion, one might expect to see a much more fulminant clinical course. This observation suggests that regulatory influences are likely to exist in this disease - a possibility supported by recent experimental data. If these regulatory influences could be identified and enhanced, specific immunotherapy for type 1 diabetes could be achieved.
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页码:61 / 69
页数:9
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