Insulitis and Exocrinitis in Autoantibody-positive Nondiabetic Individuals: Role of HLA Genotypes
Authors' conclusion
Contrary to stage 3 T1D, autoantibody-positive donors had normal β-cell mass and no significant insulitis, suggesting heterogeneity in the progression of autoimmunity, even in the presence of genetic risk, rather than a uniform slow-progressing process.
Study context
- Population
- Nondiabetic organ donors positive for ≥1 autoantibody, nPOD; median age 25 years (IQR 21–39), median BMI 24 kg/m² (21–30)117 pancreatic slides
- Participants
- 30 participants
- Exposure
- HLA at-risk vs protective vs neutral haplotypes
- Outcome
- CD3+ lymphocyte infiltration of endocrine and exocrine pancreas, according to HLA
Methodological detailsorgan donor pancreatic tissue, nPOD
- Organ donor pancreatic tissue
- nPOD
Main finding
As reported in the abstract
CD3+ lymphocyte infiltration by HLA
Insulitis identified
1 case
Observational data: associations, not effects.
Further findings
Autoantibody number
- Single autoantibody-positive
- 23
- Positive for 2 autoantibodies
- 7
β-cell mass
- β-cell mass normal in all
HLA-DQ allele distribution
- Similar to autoantibody-negative nondiabetic nPOD donors; differed from nPOD donors with stage 3 T1D
Original publication
Insulitis and Exocrinitis in Autoantibody-positive Nondiabetic Individuals: Role of HLA Genotypes. J Clin Endocrinol Metab. Published 28 January 2025. doi:10.
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