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

Paul A Lyons; Wayne W Hancock; Paul Denny; Christopher J Lord; Natasha J Hill; Nicola Armitage; Thorsten Siegmund; John A Todd; Michael S Phillips; J Fred Hess; Shiow-Ling Chen; Paul A Fischer; Laurence B Peterson; Linda S Wicker

doi:10.1016/S1074-7613(00)00012-1

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

Paul A Lyons, Wayne W Hancock, Paul Denny, Christopher J Lord, Natasha J Hill, Nicola Armitage, Thorsten Siegmund, John A Todd, Michael S Phillips, J Fred Hess, Shiow-Ling Chen, Paul A Fischer, Laurence B Peterson, Linda S Wicker

Research output: Contribution to journal › Article › peer-review

Abstract

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, Idd9 on mouse chromosome 4, is provided here by the development of a novel congenic mouse strain, NOD.B10 Idd9. NOD.B10 Idd9 mice display profound resistance to diabetes even though nearly all develop insulitis. Subcongenic analysis has demonstrated that alleles of at least three B10 genes, Idd9.1, Idd9.2, and Idd9.3 are required to produce Idd9-mediated diabetes resistance. Candidate genes with amino acid differences between the NOD and B10 strains have been localized to the 5.6 cM Idd9.2 interval (Tnfr2, Cd30) and to the 2.0 cM Idd9.3 interval (Cd137).

Original language	English
Pages (from-to)	107-115
Journal	Immunity
Volume	13
Issue number	1
DOIs	https://doi.org/10.1016/S1074-7613(00)00012-1
Publication status	Published - 1 Jul 2000
Externally published	Yes

Bibliographical note

Note: This work was supported by the Wellcome Trust, the Juvenile Diabetes Foundation, and Merck Research Laboratories.

Keywords

Allied health professions and studies

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10.1016/S1074-7613(00)00012-1

https://doi.org/10.1016/S1074-7613(00)00012-1

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Lyons, P. A., Hancock, W. W., Denny, P., Lord, C. J., Hill, N. J., Armitage, N., Siegmund, T., Todd, J. A., Phillips, M. S., Hess, J. F., Chen, S.-L., Fischer, P. A., Peterson, L. B., & Wicker, L. S. (2000). The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137. Immunity, 13(1), 107-115. https://doi.org/10.1016/S1074-7613(00)00012-1

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

abstract = "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, Idd9 on mouse chromosome 4, is provided here by the development of a novel congenic mouse strain, NOD.B10 Idd9. NOD.B10 Idd9 mice display profound resistance to diabetes even though nearly all develop insulitis. Subcongenic analysis has demonstrated that alleles of at least three B10 genes, Idd9.1, Idd9.2, and Idd9.3 are required to produce Idd9-mediated diabetes resistance. Candidate genes with amino acid differences between the NOD and B10 strains have been localized to the 5.6 cM Idd9.2 interval (Tnfr2, Cd30) and to the 2.0 cM Idd9.3 interval (Cd137).",

keywords = "Allied health professions and studies",

author = "Lyons, \{Paul A\} and Hancock, \{Wayne W\} and Paul Denny and Lord, \{Christopher J\} and Hill, \{Natasha J\} and Nicola Armitage and Thorsten Siegmund and Todd, \{John A\} and Phillips, \{Michael S\} and Hess, \{J Fred\} and Shiow-Ling Chen and Fischer, \{Paul A\} and Peterson, \{Laurence B\} and Wicker, \{Linda S\}",

note = "Note: This work was supported by the Wellcome Trust, the Juvenile Diabetes Foundation, and Merck Research Laboratories.",

year = "2000",

month = jul,

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doi = "10.1016/S1074-7613(00)00012-1",

language = "English",

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Lyons, PA, Hancock, WW, Denny, P, Lord, CJ, Hill, NJ, Armitage, N, Siegmund, T, Todd, JA, Phillips, MS, Hess, JF, Chen, S-L, Fischer, PA, Peterson, LB & Wicker, LS 2000, 'The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137', Immunity, vol. 13, no. 1, pp. 107-115. https://doi.org/10.1016/S1074-7613(00)00012-1

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T1 - The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137

AU - Lyons, Paul A

AU - Hancock, Wayne W

AU - Denny, Paul

AU - Lord, Christopher J

AU - Hill, Natasha J

AU - Armitage, Nicola

AU - Siegmund, Thorsten

AU - Todd, John A

AU - Phillips, Michael S

AU - Hess, J Fred

AU - Chen, Shiow-Ling

AU - Fischer, Paul A

AU - Peterson, Laurence B

AU - Wicker, Linda S

N1 - Note: This work was supported by the Wellcome Trust, the Juvenile Diabetes Foundation, and Merck Research Laboratories.

PY - 2000/7/1

Y1 - 2000/7/1

N2 - 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, Idd9 on mouse chromosome 4, is provided here by the development of a novel congenic mouse strain, NOD.B10 Idd9. NOD.B10 Idd9 mice display profound resistance to diabetes even though nearly all develop insulitis. Subcongenic analysis has demonstrated that alleles of at least three B10 genes, Idd9.1, Idd9.2, and Idd9.3 are required to produce Idd9-mediated diabetes resistance. Candidate genes with amino acid differences between the NOD and B10 strains have been localized to the 5.6 cM Idd9.2 interval (Tnfr2, Cd30) and to the 2.0 cM Idd9.3 interval (Cd137).

AB - 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, Idd9 on mouse chromosome 4, is provided here by the development of a novel congenic mouse strain, NOD.B10 Idd9. NOD.B10 Idd9 mice display profound resistance to diabetes even though nearly all develop insulitis. Subcongenic analysis has demonstrated that alleles of at least three B10 genes, Idd9.1, Idd9.2, and Idd9.3 are required to produce Idd9-mediated diabetes resistance. Candidate genes with amino acid differences between the NOD and B10 strains have been localized to the 5.6 cM Idd9.2 interval (Tnfr2, Cd30) and to the 2.0 cM Idd9.3 interval (Cd137).

KW - Allied health professions and studies

UR - https://www.ncbi.nlm.nih.gov/pubmed/10933399

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DO - 10.1016/S1074-7613(00)00012-1

M3 - Article

C2 - 10933399

SN - 1074-7613

VL - 13

SP - 107

EP - 115

JO - Immunity

JF - Immunity

IS - 1

ER -

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

Abstract

Bibliographical note

Keywords

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