The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137

被引：145

作者：

Lyons, PA

Hancock, WW

Denny, P

Lord, CJ

Hill, NJ

Armitage, N

Siegmund, T

Todd, JA

Phillips, MS

Hess, JF

Chen, SL

Fischer, PA

Peterson, LB

Wicker, LS ^{[1
]}

机构：

[1] Merck Res Labs, Dept Immunol & Rheumatol, Rahway, NJ 07065 USA

[2] Merck Res Labs, Dept Pharmacol, Rahway, NJ 07065 USA

[3] New England Deaconess Hosp, Sandoz Ctr Immunobiol, Boston, MA 02215 USA

[4] Harvard Univ, Sch Med, Boston, MA 02215 USA

[5] Univ Cambridge, Wellcome Trust Ctr Mol Mech, Cambridge CB2 2XY, England

[6] Merck Res Labs, Dept Human Genet, W Point, PA 19486 USA

[7] New England Deaconess Hosp, Dept Pathol, Boston, MA 02215 USA

来源：

IMMUNITY | 2000年 / 13卷 / 01期

基金：

英国惠康基金;

关键词：

D O I：

10.1016/S1074-7613(00)00012-1

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Previous analyses of NOD mice have shown that some genes control the development of both insulitis and diabetes, while other loci influence diabetes without reducing insulitis. Evidence for the existence of a gene only influencing diabetes, ldd9 on mouse chromosome 4, is provided here by the development of a novel congenic mouse strain, NOD.B10ldd9. NOD.B10ldd9 mice display profound resistance to diabetes even though nearly all develop insulitis. Subcongenic analysis has demonstrated that alleles of at least three B10 genes, ldd9.1, ldd9.2, and ldd9.3 are required to produce ldd9-mediated diabetes resistance. Candidate genes with amino acid differences between the NOD and B10 strains have been localized to the 5.6 cM ldd9.2 interval (Tnfr2, Cd30) and to the 2.0 cM ldd9.3 interval (Cd137).

引用

页码：107 / 115

页数：9

共 49 条

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