ESPE2018 Poster Presentations Diabetes & Insulin P1 (53 abstracts)
Department of Pediatric Endocrinology and Diabetology Medical University of Lublin, Lublin, Poland
Background: Regulatory T cells (Treg) of phenotype CD4+CD25+FoxP3+ involves active suppression of excessive immune response. The population of Treg cells from patients with type 1 diabetes (DM1) have numeric and functional abnormalities. Although there are many reports of investigations on human and animal populations, the role of regulatory T cells in the development of type 1 diabetes is still unclear.
Objective and hypotheses: The aim of the study is to compare the population of regulatory T cells and the correlation between Treg cells and beta cells autoantibody in healthy siblings of children with DM1 to healthy children from non-diabetic families and to children with DM1.
Method: Peripheral blood mononuclear blood cells were obtained from 76 children with DM1, their siblings 101, and 30 healthy children. Treg cells were characterized by flow cytometry FACSCalibur (Becton Dickinson, USA). The auto-antibodies were determined by ELISA. The results were analyzed with STATISTICA 10 PL.
Results: The number of regulatory T cells from diabetic patients was higher (average percentage 0.23±0.20) than that in the siblings (0.15±0.14) (P=0.004). There was no significant difference in the number of Treg cells between children with DM1 and the control group (0.19±0.15; P=0.11) and between siblings and the control group (P=0.09). The levels of anti IA2 and anti ZnT8 antibodies were statistically significant higher in siblings in comparison to the control group (anti IA2 Ab P=0.0000001; anti ZnT8 Ab P=0.00001). The level of anti-GAD in siblings was similar to that in the control group. There was no correlation between the number of Treg cells and the co-occurrence of beta cells auto-antibody.
Conclusion: The results suggest that regulatory T cells probably provide protection from development of disease and the dysfunction of Treg cells contributes to the autoimmune pathogenesis of type 1 diabetes.