Causal Effect of Type 1 Diabetes on Juvenile Idiopathic Arthritis and the Mediating Role of CD8+ Natural Killer T Cells
Authors' conclusion
The study confirmed a significant causal effect of T1D on JIA from a genetic perspective, revealed CD8+ NKT cells as a pivotal mediating factor in this causal pathway, and verified a predisposition to inflammatory arthritis in young NOD mice.
Study context
- Comparison
- Genetic liability to T1D and juvenile idiopathic arthritis
- Outcome
- Causal effect of T1D on JIA
Methodological detailslinkage disequilibrium score regression, mediation analysis, in vivo mouse models (nonobese diabetic (NOD), streptozotocin (STZ)-induced diabetic, mannan-induced arthritic mice)
- Linkage disequilibrium score regression
- Mediation analysis
- In vivo mouse models (NOD, STZ-induced diabetic, mannan-induced arthritic mice)
Main finding
As reported in the abstract
CD8+ natural killer T (NKT) absolute count had a significant mediating effect; proportion of increased juvenile idiopathic arthritis (JIA) risk attributable to T1D mediated
32.5%
Further findings
Arthritis in mouse models
- Young NOD mice spontaneously developed mild osteoarthritis and progressive synovitis, with systemic inflammation
- No signs of osteoarthritis or synovitis in young STZ-induced diabetic mice
- CD8+ NKT cell count negatively associated with development of mannan-induced arthritis in SKG mice
Original publication
Causal Effect of Type 1 Diabetes on Juvenile Idiopathic Arthritis and the Mediating Role of CD8+ Natural Killer T Cells. J Clin Endocrinol Metab. Published 15 December 2025. doi:10.
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