Genetic control of diabetes progression

被引：124
作者：
Gonzalez, A
Katz, JD
Mattei, MG
Kikutani, H
Benoist, C
Mathis, D
机构：
[1] CNRS INSERM, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, Strasbourg, France
[2] Fac Med Timone, INSERM, U406, F-13385 Marseille 5, France
[3] Osaka Univ, Microbial Dis Res Inst, Div Mol Immunol, Suita, Osaka 565, Japan
来源：
IMMUNITY | 1997年 / 7卷 / 06期
关键词：
D O I：
10.1016/S1074-7613(00)80405-7
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Autoimmune diabetes in both the human and the nonobese diabetic mouse has elaborate genetics; in the latter case, the disease is influenced by at least 15-20 loci. We anticipated that the genetics would be simpler in the BDC2.5 T cell receptor transgenic mouse model of diabetes, wherein many T cells express a particular diabetogenic specificity. Initiation of insulitis in this model was the same on the two genetic backgrounds analyzed, but the kinetics and penetrance of diabetes were strikingly different, permitting us to focus on genetic influences during a defined window of disease progression. The differences correlated with variations in five genomic intervals, certain ones of which have been previously implicated in susceptibility to autoimmune disease. This reductionist approach indeed simplified the analysis of diabetes susceptibility loci.
引用
收藏
页码：873 / 883
页数：11
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