Druggable targets and immunological mechanisms for type 1 diabetes treatment: Genetic evidence from multi‐omics Mendelian randomization combined with meta‐analysis
Authors' conclusion
This study used a Mendelian randomization approach to provide genetic evidence, providing insights and direction for the development of preventive and therapeutic drugs for T1DM.
Study context
- Population
- Large T1D GWAS data; QTL from three discovery datasets representing druggable targets; 731 immune cell types
- Outcome
- Causal association of druggable targets with T1D
Methodological detailsmulti-omics, drug-target mendelian randomization (MR), Bayesian colocalization, mediation analysis, PheWAS
- Multi-omics
- Drug-target MR
- Bayesian colocalization
- Mediation analysis
- PheWAS
Pooled result
As reported in the abstract
Druggable targets for T1D
- Potential druggable targets for T1D identified
- 11
Further pooled results
Mediation of CTSH effect on T1D by myeloid cells (CD33dim HLA-DR+ CD11b-)
| OR (95% CI) | P value | ||
|---|---|---|---|
| CD33dim HLA-DR+ CD11b- myeloid cells (mediator of CTSH) | 1.014 (1.004–1.024) | P = 0.008 | |
| 0.512Odds ratio (log scale) |
- Mediation of CTSH effect on T1D by myeloid cells (CD33dim HLA-DR+ CD11b-) — Mediation proportion
- 8.3%
PheWAS
- NAGA, NAAA, ITIH3 and CTSH may influence additional phenotypes
Original publication
Druggable targets and immunological mechanisms for type 1 diabetes treatment: Genetic evidence from multi‐omics Mendelian randomization combined with meta‐analysis. Diabet Med. Published 21 December 2025. doi:10.
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