Genetic evidence for efficacy of targeting IL-2, IL-6 and TYK2 signalling in the prevention of type 1 diabetes: a Mendelian randomisation study
Authors' conclusion
Our findings support the targeting of IL-2, IL-6 and TYK2 signalling in prevention of type 1 diabetes.
Study context
- Population
- GWAS summary statistics for T1D risk, whole-blood gene expression and serum protein levels; polymorphisms near seven potential drug target genes
- Comparison
- Genetically proxied expression of drug target genes vs T1D risk
- Outcome
- T1D risk per 1-SD increase in genetically proxied drug target gene expression
Methodological detailsco-localisation, drug target genetic proxies, functional (missense) variant analysis
- Co-localisation
- Drug target genetic proxies
- Functional (missense) variant analysis
Main finding
As reported in the abstract
T1D risk per 1-SD increase in genetically proxied gene expression
IL2RA expression: OR
0.22 (0.17, 0.27) (95% CI)
IL6R expression: OR
1.98 (1.48, 2.65) (95% CI)
IL6ST expression: OR
1.90 (1.45, 2.48) (95% CI)
TYK2 expression (missense variants): OR
0.61 (0.54, 0.69) (95% CI)
Further findings
Co-localisation of blood expression with T1D liability (shared causal variant)
- IL2RA: posterior probability
- 100%
- IL6R: posterior probability
- 96.5%
- IL6ST: posterior probability
- 97.0%
Original publication
Genetic evidence for efficacy of targeting IL-2, IL-6 and TYK2 signalling in the prevention of type 1 diabetes: a Mendelian randomisation study. Diabetologia. Published 13 September 2024. doi:10.
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