Integrating immune-cell transcriptomic data with Mendelian randomisation reveals novel causal genes for type 2 diabetes and its complications
Authors' conclusion
Our study supports a key role for immune mechanisms in diabetic complications and highlights promising therapeutic targets by distinguishing and minimising the influence of cell-type-related pleiotropy.
Study context
- Population
- T2D and its complications; 18,611 immune expression quantitative trait loci (eQTL) of 4487 genes
- Outcome
- Immune-cell gene expression causally associated with T2D and its complications (MR and colocalisation)
Methodological detailscolocalisation, multivariable Mendelian randomisation (MR), clustering analyses, immune eQTL
- Colocalisation
- Multivariable MR
- Clustering analyses
- Immune eQTL
Main finding
As reported in the abstract
- Unique genes whose expression was associated with T2D
- 425
- Unique genes whose expression was associated with T2D complications
- 123
- Pleiotropic genes, classic pleiotropy
- 40.0%
- Pleiotropic genes, classic and/or cell-type-related pleiotropy
- 71.1%
- Immune-related drug targets prioritised for diabetic complications
- 10
Original publication
Integrating immune-cell transcriptomic data with Mendelian randomisation reveals novel causal genes for type 2 diabetes and its complications. Diabetologia. Published 12 May 2026. doi:10.
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