ArticleDiabetologia2024
Genetic evidence for efficacy of targeting IL-2, IL-6 and TYK2 signalling in the prevention of type 1 diabetes: a Mendelian randomisation study.
Article in Diabetologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Role ofInternational journal of molecular sciences · 2026Article
- Causal Risk Factors for Type 1 Diabetes in Mendelian Randomization Studies: A Systematic Review and Meta-Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- The Contribution of BMI to a Young Child's Risk of Islet Autoimmunity Is Dependent on HLA-DR4-DQ8 Without HLA-DR3-DQ2.Diabetes care · 2025Article
- Genetic analysis of the correlation between GLP1 action and metabolic liver disease: Insights from Mendelian randomization analysis.Journal of diabetes investigation · 2025Article
- Exploring autism spectrum disorder and co-occurring trait associations to elucidate multivariate genetic mechanisms and insights.BMC psychiatry · 2024Article
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6 authors.
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Abstract
aims/hypothesisWe aimed to investigate the genetic evidence that supports the repurposing of drugs already licensed or in clinical phases of development for prevention of type 1 diabetes.
methodsWe obtained genome-wide association study summary statistics for the risk of type 1 diabetes, whole-blood gene expression and serum protein levels and investigated genetic polymorphisms near seven potential drug target genes. We used co-localisation to examine whether the same genetic variants that are associated with type 1 diabetes risk were also associated with the relevant drug target genetic proxies and used Mendelian randomisation to evaluate the direction and magnitude of the associations. Furthermore, we performed Mendelian randomisation analysis restricted to functional variants within the drug target genes.
resultsCo-localisation revealed that the blood expression levels of IL2RA (encoding IL-2 receptor subunit α [IL2RA]), IL6R (encoding IL-6 receptor [IL6R]) and IL6ST (encoding IL-6 cytokine family signal transducer [IL6ST]) shared the same causal variant with type 1 diabetes liability near the corresponding genes (posterior probabilities 100%, 96.5% and 97.0%, respectively). The OR (95% CI) of type 1 diabetes per 1-SD increase in the genetically proxied gene expression of IL2RA, IL6R and IL6ST were 0.22 (0.17, 0.27), 1.98 (1.48, 2.65) and 1.90 (1.45, 2.48), respectively. Using missense variants, genetically proxied TYK2 (encoding tyrosine kinase 2) expression levels were associated with type 1 diabetes risk (OR 0.61 [95% CI 0.54, 0.69]). CONCLUSIONS/
interpretationOur findings support the targeting of IL-2, IL-6 and TYK2 signalling in prevention of type 1 diabetes. DATA AVAILABILITY: The analysis code is available at https://github.com/jkoskenniemi/T1DSCREEN , which also includes instructions on how to download the original GWAS summary statistics.
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