ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Genetic interactions among Idd3, Idd5.1, Idd5.2, and Idd5.3 protective loci in the nonobese diabetic mouse model of type 1 diabetes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- ACADL-YAP axis activity in non-small cell lung cancer carcinogenicity.Cancer cell international · 2024Article
- Autoimmune-Disease-Prone NOD Mice Help To Reveal a New Genetic Locus for Reducing Pulmonary Disease Caused by Mycoplasma pulmonis.Infection and immunity · 2018Article
- Acyl-CoA dehydrogenase long chain expression is associated with esophageal squamous cell carcinoma progression and poor prognosis.OncoTargets and therapy · 2018Article
- c-Src kinase is involved in the tyrosine phosphorylation and activity of SLC11A1 in differentiating macrophages.PloS one · 2018Article
- The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Frontiers in endocrinology · 2018Article
- Plethysmography Phenotype QTL in Mice Before and After Allergen Sensitization and Challenge.G3 (Bethesda, Md.) · 2016Article
- Reduced interleukin-2 responsiveness impairs the ability of Treg cells to compete for IL-2 in nonobese diabetic mice.Immunology and cell biology · 2016Article
- [Roles of interleukin-21 and its receptor in autoimmune diseases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Review
- Article
- Type 1 Diabetes Prone NOD Mice Have Diminished Cxcr1 mRNA Expression in Polymorphonuclear Neutrophils and CD4+ T Lymphocytes.PloS one · 2015Article
- Increased autoimmune diabetes in pIgR-deficient NOD mice is due to a "Hitchhiking" interval that refines the genetic effect of Idd5.4.PloS one · 2015Article
- Pathway-guided identification of gene-gene interactions.Annals of human genetics · 2014Article
- Congenic mice reveal genetic epistasis and overlapping disease loci for autoimmune diabetes and listeriosis.Immunogenetics · 2014Article
- Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.PloS one · 2014Article
- Analysis of gene-gene interactions using gene-trait similarity regression.Human heredity · 2014Article
- Functional validation of the genetic architecture of Salmonella Enteritidis persistence in 129S6 mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
In the NOD mouse model of type 1 diabetes, insulin-dependent diabetes (Idd) loci control the development of insulitis and diabetes. Independently, protective alleles of Idd3/Il2 or Idd5 are able to partially protect congenic NOD mice from insulitis and diabetes, and to partially tolerize islet-specific CD8(+) T cells. However, when the two regions are combined, mice are almost completely protected, strongly suggesting the existence of genetic interactions between the two loci. Idd5 contains at least three protective subregions/causative gene candidates, Idd5.1/Ctla4, Idd5.2/Slc11a1, and Idd5.3/Acadl, yet it is unknown which of them interacts with Idd3/Il2. Through the use of a series of novel congenic strains containing the Idd3/Il2 region and different combinations of Idd5 subregion(s), we defined these genetic interactions. The combination of Idd3/Il2 and Idd5.3/Acadl was able to provide nearly complete protection from type 1 diabetes, but all three Idd5 subregions were required to protect from insulitis and fully restore self-tolerance. By backcrossing a Slc11a1 knockout allele onto the NOD genetic background, we have demonstrated that Slc11a1 is responsible for the diabetes protection resulting from Idd5.2. We also used Slc11a1 knockout-SCID and Idd5.2-SCID mice to show that both loss-of-function alleles provide protection from insulitis when expressed on the SCID host alone. These results lend further support to the hypothesis that Slc11a1 is Idd5.2.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.