Programmed cell death-1, is dysregulated in T cells from children with new onset type-1 diabetes.


eMedinexuS editorial    13 September 2017

It is known that programmed death cell-1 (PD-1) is an inhibitor of T cell activation and is also functionally linked to glycolysis.

A new study published in PLoS One hypothesized that PD-1 expression is defective in activated T cells from children with type-1 diabetes (T1D), resulting in abnormal T cell glucose metabolism. In this pilot study, children with new onset T1D within 2 weeks of diagnosis (T1D); unaffected siblings of T1D (SIBS); unaffected, unrelated children (CTRL); children with new onset; and untreated children with Crohn’s disease (CD) were enrolled. In these subjects, essays were repeated 4-6 months post-diagnosis in T1D (T1D follow up).

Overall, 37 children were included. It was observed that T cells derived from subjects with T1D had decreased PD-1 expression than those from other study groups. On the other hand, in T1D follow-up, T cells expressed PD-1 similar to controls, but had no differences in peripheral blood mononuclear cell (PBMC) cytokine production. While, T1D follow up PBMCs had enhanced glycolytic capacity compared to T1D.

From the findings, it was inferred that activated T cells from T1D fail to upregulate PD-1 upon T-cell receptor stimulation, which may contribute to the pathogenesis of T1D. T1D follow up PBMC expression of PD-1 normalizes, together with a significant increase in glycolysis compared to T1D. Thus, it was stated that insulin therapy in T1D children is associated with normal PD1 expression and heightened glycolytic capacity in PBMC.

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