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胰腺白细胞介素-10在NOD.B6 Idd3 Idd10小鼠中诱发糖尿病。

Pancreatic IL-10 induces diabetes in NOD.B6 Idd3 Idd10 mice.

作者信息

Lee M S, Wicker L S, Peterson L B, Sarvetnick N

机构信息

Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037, USA.

出版信息

Autoimmunity. 1997;26(4):215-21. doi: 10.3109/08916939709008027.

Abstract

Transgenic NOD backcross mice expressing pancreatic interleukin 10 (IL-10) were crossed and backcrossed to NOD.B6 Idd3 Idd10 mice, which have diabetes-resistance alleles at Idd3 and Idd10 on chromosome 3 and have a very low frequency diabetes and insulitis. Insulitis and diabetes developed in almost all IL-10 transgenic backcross 1 (BC1) mice of the H2g(7/g7) haplotype regardless of the allelic status at Idd3 and Idd10. Furthermore, diabetes occurred in 23% of IL-10 transgenic H2g(7/d) BC1 mice. These results indicate that pancreatic IL-10 is able to overcome the diabetes protection afforded by C57BL/6 (B6)-derived alleles at Idd3 and Idd10 as well as the absence of NOD MHC homozygosity, if other non-MHC NOD-derived Idd alleles are provided.

摘要

将表达胰腺白细胞介素10(IL-10)的转基因NOD回交小鼠与NOD.B6 Idd3 Idd10小鼠进行杂交和回交,后者在3号染色体的Idd3和Idd10位点具有抗糖尿病等位基因,糖尿病和胰岛炎的发生率很低。几乎所有H2g(7/g7)单倍型的IL-10转基因回交1(BC1)小鼠都发生了胰岛炎和糖尿病,而与Idd3和Idd10的等位基因状态无关。此外,23%的IL-10转基因H2g(7/d) BC1小鼠发生了糖尿病。这些结果表明,如果提供其他非MHC的NOD来源的Idd等位基因,胰腺IL-10能够克服Idd3和Idd10位点上C57BL/6(B6)来源的等位基因以及缺乏NOD MHC纯合性所提供的糖尿病保护作用。

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