ArticleDiabetes2005
The rat diabetes susceptibility locus Iddm4 and at least one additional gene are required for autoimmune diabetes induced by viral infection.
Article in Diabetes, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Deletion of Vβ3Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Genetics of murine type 2 diabetes and comorbidities.Mammalian genome : official journal of the International Mammalian Genome Society · 2022Review
- A Critical Role for the Type I Interferon Receptor in Virus-Induced Autoimmune Diabetes in Rats.Diabetes · 2017Article
- Autoantigen-induced focusing of Vβ13+ T cells precedes onset of autoimmune diabetes in the LEW.1WR1 rat.Diabetes · 2014Article
- The Missing Heritability in T1D and Potential New Targets for Prevention.Journal of diabetes research · 2013Article
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- Genetic dissection reveals diabetes loci proximal to the gimap5 lymphopenia gene.Physiological genomics · 2009Article
- Type 1 diabetes in the BB rat: a polygenic disease.Diabetes · 2009Article
- Analysis of the rat Iddm14 diabetes susceptibility locus in multiple rat strains: identification of a susceptibility haplotype in the Tcrb-V locus.Mammalian genome : official journal of the International Mammalian Genome Society · 2009Article
- CHOP mediates endoplasmic reticulum stress-induced apoptosis in Gimap5-deficient T cells.PloS one · 2009Article
- Review
- A novel susceptibility locus on rat chromosome 8 affects spontaneous but not experimentally induced type 1 diabetes.Diabetes · 2007Article
- Diubiquitin (Ubd) is a susceptibility gene for virus-triggered autoimmune diabetes in rats.Genes and immunityArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
BBDR rats develop autoimmune diabetes only after challenge with environmental perturbants. These perturbants include polyinosinic:polycytidylic acid (poly I:C, a ligand of toll-like receptor 3), agents that deplete regulatory T-cell (Treg) populations, and a non-beta-cell cytopathic parvovirus (Kilham rat virus [KRV]). The dominant diabetes susceptibility locus Iddm4 is required for diabetes induced by treatment with poly I:C plus Treg depletion. Iddm4 is penetrant in congenic heterozygous rats on the resistant WF background and is 79% sensitive and 80% specific as a predictor of induced diabetes. Surprisingly, an analysis of 190 (BBDR x WF)F2 rats treated with KRV after brief exposure to poly I:C revealed that the BBDR-origin allele of Iddm4 is necessary but not entirely sufficient for diabetes expression. A genome scan identified a locus on chromosome 17, designated Iddm20, that is also required for susceptibility to diabetes after exposure to KRV and poly I:C (logarithm of odds score 3.7). These data suggest that the expression of autoimmune diabetes is a complex process that requires both major histocompatibility complex genes that confer susceptibility and additional genes such as Iddm4 and Iddm20 that operate only in the context of specific environmental perturbants, amplifying the immune response and the rate of disease progression.
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