GENETIC REQUIREMENTS FOR ACCELERATION OF DIABETES IN NONOBESE DIABETIC MICE EXPRESSING INTERLEUKIN-2 IN ISLET BETA-CELLS

被引：30

作者：

ALLISON, J ^{[1
]}

MCCLIVE, P ^{[1
]}

OXBROW, L ^{[1
]}

BAXTER, A ^{[1
]}

MORAHAN, G ^{[1
]}

MILLER, JFAP ^{[1
]}

机构：

[1] UNIV SYDNEY, CENTENARY INST CANC MED & CELL BIOL, SYDNEY, NSW 2006, AUSTRALIA

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 1994年 / 24卷 / 10期

关键词：

INTERLEUKIN-2 TRANSGENIC MICE; NONOBESE DIABETIC MICE; AUTOIMMUNITY; DIABETES SUSCEPTIBILITY GENES; CYTOKINES;

D O I：

10.1002/eji.1830241041

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Diabetes was dramatically accelerated in non-obese diabetic (NOD) transgenic mice that expressed interleukin-2 (IL-2) in their beta cells. A single cross to C57BL/6 completely prevented this effect and a further backcross to the NOD genetic background showed that at least two diabetes susceptibility loci (Idd1s and Idd3/10s) were required for the diabetes acceleration. T cells activated to islet antigens were not circulating in the mice. The accelerating effect of IL-2 was present, but decreased, in NOD mice that lacked CD8(+) T cells as well as in NOD SCID mice. The implications are that in the NOD genetic background, the production of cytokines, such as IL-2, by islet-specific CD4(+) T cells can lead to beta cell damage and diabetes and that CD8(+) T cells may have a role in accelerating diabetes onset.

引用

页码：2535 / 2541

页数：7

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