ReviewThe review of diabetic studies : RDS2012
Comparative genetics: synergizing human and NOD mouse studies for identifying genetic causation of type 1 diabetes.
Review in The review of diabetic studies : RDS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- The influence of ICAM1 rs5498 on diabetes mellitus risk: evidence from a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Pooled it
- Receptor-tethered orthogonal IL-2 enhances regulatory T cell therapy.The Journal of experimental medicine · 2026Article
- From pancreas and islet resources to diabetes insights.Diabetologia · 2026Review
- A streamlined approach for gene editing in non-obese diabetes (NOD) mice via CRISPR/Cas9.Laboratory animal research · 2026Article
- The Genetic Landscape of Diabetes Mellitus: Lessons from Monogenic and Polygenic Forms.Life (Basel, Switzerland) · 2026Review
- Immune cell-adipose tissue crosstalk in metabolic diseases with a focus on type 1 diabetes.Diabetologia · 2025Review
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Regulatory T Cell Insufficiency in Autoimmune Diabetes Is Driven by Selective Loss of Neuropilin-1 on Intraislet Regulatory T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Untangling the genetics of beta cell dysfunction and death in type 1 diabetes.Molecular metabolism · 2024Review
- Deletion of Vβ3Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Islet beta-cells and intercellular adhesion molecule-1 (ICAM-1): Integrating immune responses that influence autoimmunity and graft rejection.Autoimmunity reviews · 2023Review
- Review
- Preclinical models for Type 1 Diabetes Mellitus - A practical approach for research.International journal of medical sciences · 2023Review
- A Distinctive γδ T Cell Repertoire in NOD Mice Weakens Immune Regulation and Favors Diabetic Disease.Biomolecules · 2022Article
- Modulation of autoimmune diabetes by N-ethyl-N-nitrosourea- induced mutations in non-obese diabetic mice.Disease models & mechanisms · 2022Article
- Preclinical Models to Evaluate the Human Response to Autoantigen and Antigen-Specific Immunotherapy in Human Type 1 Diabetes.Frontiers in endocrinology · 2022Review
- The long and winding road: From mouse linkage studies to a novel human therapeutic pathway in type 1 diabetes.Frontiers in immunology · 2022Review
- Intergenomic and epistatic interactions control free radical mediated pancreatic β-cell damage.Frontiers in genetics · 2022Article
- Construction of 3D hierarchical tissue platforms for modeling diabetes.APL bioengineering · 2021Review
- Noncontiguous T cell epitopes in autoimmune diabetes: From mice to men and back again.The Journal of biological chemistry · 2021Review
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 1 institution in 1 country.
Funding
Abstract
Although once widely anticipated to unlock how human type 1 diabetes (T1D) develops, extensive study of the nonobese diabetic (NOD) mouse has failed to yield effective treatments for patients with the disease. This has led many to question the usefulness of this animal model. While criticism about the differences between NOD and human T1D is legitimate, in many cases disease in both species results from perturbations modulated by the same genes or different genes that function within the same biological pathways. Like in humans, unusual polymorphisms within an MHC class II molecule contributes the most T1D risk in NOD mice. This insight supports the validity of this model and suggests the NOD has been improperly utilized to study how to cure or prevent disease in patients. Indeed, clinical trials are far from administering T1D therapeutics to humans at the same concentration ranges and pathological states that inhibit disease in NOD mice. Until these obstacles are overcome it is premature to label the NOD mouse a poor surrogate to test agents that cure or prevent T1D. An additional criticism of the NOD mouse is the past difficulty in identifying genes underlying T1D using conventional mapping studies. However, most of the few diabetogenic alleles identified to date appear relevant to the human disorder. This suggests that rather than abandoning genetic studies in NOD mice, future efforts should focus on improving the efficiency with which diabetes susceptibility genes are detected. The current review highlights why the NOD mouse remains a relevant and valuable tool to understand the genes and their interactions that promote autoimmune diabetes and therapeutics that inhibit this disease. It also describes a new range of technologies that will likely transform how the NOD mouse is used to uncover the genetic causes of T1D for years to come.
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What OpenQuestion holds
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.