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• W2154144468 abstract "Type 1 diabetes is an autoimmune disease in which insulin-producing beta cells are destroyed by auto-reactive T lymphocytes. Studies in mice indicate that incomplete deletion of self-reactive T-cells and compromised peripheral tolerance mechanisms can contribute to the manifestation of autoimmune diabetes. In patients with type 1 diabetes, defects in T regulatory cell numbers and function have been previously reported. In this study, we have ascertained the integrity of activation-induced cell death, a mechanism of peripheral T cell tolerance, in long-standing type 1 diabetes patients. Activation of peripheral blood derived T cells from non-diabetic individuals with a T cell mitogen and interleukin-2 rendered them susceptible to subsequent T-cell receptor/CD3mediated apoptosis, as indicated by the dissipation of the mitochondrial membrane potential and activation of intracellular caspases. In contrast, similarly activated T lymphocytes from type 1 diabetes patients failed to undergo apoptosis when challenged with a bacterial superantigen or anti-CD3 antibody. Supplementation of T cell cultures with interleukin-4 or interleukin-18 failed to restore self-tolerance. However, both the expression of the Fas receptor and its ability to transduce apoptotic signal were comparable in T cells of type 1 diabetes patients and controls. Additionally, no marked difference in the T cell subsets was observed between controls and diabetes patients under all activation conditions analyzed. These data suggest that the abnormality in T-cell receptor-mediated apoptosis is cell autonomous in long-standing type 1 diabetes patients, which in addition to other defective peripheral tolerance mechanisms, likely to contribute to the manifestation of autoimmune diabetes." @default.
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• W2154144468 date "2012-07-03" @default.
• W2154144468 modified "2023-09-27" @default.
• W2154144468 title "Patients with Type 1 Diabetes Display Selective Defect in Antigen Receptor Mediated T Cell Apoptosis" @default.
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