Abstract

Type 1 diabetes (T1D) is the result of the autoimmune destruction of insulin-producing beta cells. Regulatory T cells (Tregs) and plasmacytoid dendritic cells ( PDCs) act as mediators of peripheral tolerance. We investigated the possible alterations of such cells in peripheral blood of patients with T1D compared to normal individuals. This comparison may lead to a better understanding of the immunopathogenesis processes involved in T1D. 92 participants, including 49 patients with T1D and 43 healthy controls were studied. 3 mL of blood was taken from all participants. After isolating peripheral blood mononuclear cells (PBMCs), PDCs as well as 2 subtypes of Tregs, CD4(+)CD25(+)FoxP3(+) and CD8(+)CD28cells were counted by 3-colorflow cytometry. The association between such enumeration and T1D was studied by multivariate regression and discriminate function models. The frequency of CD4(+)CD25(+)FoxP3(+)Tregs (p=0.038) and PDCs ( p=0.039) in the peripheral blood of diabetic patients was less than that in healthy subjects. Having compared some models consisting different cells as well as their combinations, we did not find any profound explanation of each subset or their combinations to identify T1D. The decrease of CD4(+)CD25(+)FoxP3(+)cells and PDCs in diabetic patients may suggest their role in the onset or development of the disease. Therefore, it is likely that their pharmacologic stimulation may direct immune responses towards tolerance and prevent the development or even the onset of diabetes in susceptible individuals.