ESPE Abstracts (2014) 82 P-D-1-1-63

aDepartment of Pediatric Endocrinology and Diabetology, Medical University of Lublin, Lublin, Poland; bDepartment of Clinical Immunology, Medical University of Lublin, Lublin, Poland


Background: A recent data indicates a complex mechanism of β-cell destruction in type 1 diabetes in which despite Th1/Th2 bias different other populations of immune cells like Th17 with specific IL17A secretion with proinflammatory action will mediate β cells autoreactivity. In humans, the relevance of Th17 cells in new onset T1DM is still controversial.

Objective and hypotheses: The aim of our study was to evaluate circulating Th17 in children with new onset type 1 diabetes and comparison to a group of healthy children.

Method: The study group comprised 53 children, mean age 10.2±5.5 years, with newly diagnosed type 1 diabetes. In all children were assessed C-peptide and anti-GAD and anti-IA2 antibodies to confirm autoimmune pathogenesis of disease and cell subpopulations were examined using flow cytometry. The reference group consisted of 20 healthy children. The percentage of circulating CD4+IL17A+ and CD4+/CD3+/IL17A+T cells with expression of Th17-related transcription factor RORγt have been analyzed.

Results: Comparison between T1DM children and healthy counterparts showed no statistically significant difference in average percentage of circulating Th17 cells but there was significant difference in mean fluorescence intensity (MFI) between studied groups (P<0.01). Interestingly, as we evaluated TH17 cells at different time points of disease progression during initial phase of diabetes (6, 30, and 60 days from diagnosis of DM) we have noted gradual statistically significant decrease (P<0.05) in the absolute number of Th17 cells with positive correlation with insulin requirement (total daily insulin dose). There were no correlation between the percentage of CD4+IL17A+ and CD4+/CD3+/IL17A+T cells and C-peptide and HbA1c level.

Conclusion: Based on these findings more detailed analysis of the observed dependence is needed but it seems that observed changes in population of Th17 cells may be due to accumulation in the target organ during the initial effector phase of type 1 diabetes.

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