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Article

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

Immunity - 1 Jul 2000

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

Abstract excerpt

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 deve...

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PMID: 10933399
DOI: 10.1016/s1074-7613(00)00012-1

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-10933399-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137.PMID 10933399Read ↗

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Congenic mapping identifies a novel Idd9 subregion regulating type 1 diabetes in NOD mice.Semantic proximity Read ↗

Analysis of the mouse CD30 gene: a candidate for the NOD mouse type 1 diabetes locus Idd9.2.Semantic proximity Read ↗

Congenic mapping of the diabetogenic locus Idd4 to a 5.2-cM region of chromosome 11 in NOD mice: identification of two potential candidate subloci.Semantic proximity Read ↗

Subcongenic analyses reveal complex interactions between distal chromosome 4 genes controlling diabetogenic B cells and CD4 T cells in nonobese diabetic mice.Semantic proximity Read ↗

Idd9.2 and Idd9.3 protective alleles function in CD4+ T-cells and nonlymphoid cells to prevent expansion of pathogenic islet-specific CD8+ T-cells.Semantic proximity Read ↗

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Genetic control of anti-Sm autoantibody production in NOD congenic mice narrowed to the Idd9.3 region.Semantic proximity Read ↗

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