ArticleFrontiers in endocrinology2018
The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.
Article in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05616273 (Stimulated Glucagon as a Biomarker of Hypoglycemic Risk in Type 1 Diabetes), which is not on this map. Cited by 85 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Stimulated Glucagon as a Biomarker of Hypoglycemic Risk in Type 1 Diabetes
Who cites it
85 citing papers in PubMed, 130 citations in OpenAlex.
- Role of small intronic RNAs in the crosstalk between immune cells and β-cells during type 1 diabetes development.RNA biology · 2026Article
- A streamlined approach for gene editing in non-obese diabetes (NOD) mice via CRISPR/Cas9.Laboratory animal research · 2026Article
- Article
- Real-time in vivo analysis of murine β cells reveals autophagic flux defects before onset of autoimmune diabetes.Science translational medicine · 2026Article
- The subset of M1-paired MHC class II conformers is critical for CD4+ T cell activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Gain-of-function mutation inbioRxiv : the preprint server for biology · 2026Article
- Review
- Strategic Reduction of Hybrid Insulin Peptide Formation Significantly Delays Diabetes Onset in NOD Mice.Diabetes · 2026Article
- Gut microbiota and pathobiont exposure influences disease incidence in non-obese diabetic mice.Frontiers in microbiology · 2026Article
- Humanized Mouse Models for Type 1 Diabetes.Current protocols · 2025Review
- ST8Sia6 overexpression protects pancreatic β cells from spontaneous autoimmune diabetes in nonobese diabetic mice.The Journal of clinical investigation · 2025Article
- T helper 17 cells and interleukin-17 immunity in type 1 diabetes: From pathophysiology to targeted immunotherapies.World journal of diabetes · 2025Review
- Characterization and effective expansion of CD4Molecular therapy. Methods & clinical development · 2025Article
- Targeted animal models for preclinical assessment of cellular and gene therapies in pancreatic and liver diseases: regulatory and practical insights.Cytotherapy · 2025Review
- From Microbes to Metabolites: Advances in Gut Microbiome Research in Type 1 Diabetes.Metabolites · 2025Review
- Mouse NOD/Shi and NSY/Hos strains infected with Plasmodium berghei ANKA are models for experimental cerebral malaria.Experimental animals · 2025Article
- Early pathological changes in the liver and kidney of non-obese diabetic (NOD) mice: involvement of iron accumulation and ferroptosis.Frontiers in endocrinology · 2025Article
- Harnessing cellular therapeutics for type 1 diabetes mellitus: progress, challenges, and the road ahead.Nature reviews. Endocrinology · 2025Review
- Article
- NOD alleles at Idd1 and Idd2 loci drive exocrine pancreatic inflammation.Immunogenetics · 2024Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
For more than 35 years, the NOD mouse has been the primary animal model for studying autoimmune diabetes. During this time, striking similarities to the human disease have been uncovered. In both species, unusual polymorphisms in a major histocompatibility complex (MHC) class II molecule confer the most disease risk, disease is caused by perturbations by the same genes or different genes in the same biological pathways and that diabetes onset is preceded by the presence of circulating autoreactive T cells and autoantibodies that recognize many of the same islet antigens. However, the relevance of the NOD model is frequently challenged due to past failures translating therapies from NOD mice to humans and because the appearance of insulitis in mice and some patients is different. Nevertheless, the NOD mouse remains a pillar of autoimmune diabetes research for its usefulness as a preclinical model and because it provides access to invasive procedures as well as tissues that are rarely procured from patients or controls. The current article is focused on approaches to improve the NOD mouse by addressing reasons why immune therapies have failed to translate from mice to humans. We also propose new strategies for mixing and editing the NOD genome to improve the model in ways that will better advance our understanding of human diabetes. As proof of concept, we report that diabetes is completely suppressed in a knock-in NOD strain with a serine to aspartic acid substitution at position 57 in the MHC class II Aβ. This supports that similar non-aspartic acid substitutions at residue 57 of variants of the human class II HLA-DQβ homolog confer diabetes risk.
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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.