LAUSR

is unknown. Therefore, we examined whether hyperglycemia alters T-cell priming by dendritic cells, and results in increased T-cell proliferation and an effector phenotype. Methods: Immature human DCs were cultured with different concentrations of glucose (5.5 mmol/L, 15 mmol/L, or 30 mmol/L) for 24 hours. Autologous T-lymphocytes (T-cells) were then added to the DC cultures in fresh media without the addition of glucose and allowed to proliferate for five days. Flow cytometry was used to investigate the immunophenotype of the DCs after culture, as well as the phenotype and degree of proliferation that T cells underwent. Results: The incubation of DCs with high amounts of glucose resulted in an increase expression of DC markers of activation, CD83, and HLA-DR. Furthermore, at a high concentration of glucose (30 mmol/mL), DCs induced T-cells with a more activated phenotype than those DCs stimulated with a physiological concentration of glucose (5.5 mmol/mL). This was evident by the loss of CD27 expression on the T-cells induced by DCs stimulated with 30 mmol/mL of glucose. Conclusion: An elevated glucose concentration leads to the maturation of DCs and increased proliferation and effector phenotype of T-cells that are subsequently encountered. These results support the hypothesis that hyperglycemia alters T-cell priming by dendritic cells, and lay the foundation for future studies aimed at elucidating therapeutic strategies that inhibit diabetes and associated inflammation but preserve immunity.