Abstract
Abstract Type-1 diabetes is an autoimmune disease caused by the destruction of insulin-producing pancreatic beta cells by auto-reactive T-cells. It results from a failure of the immune system to maintain tolerance to self-antigens. CD4+CD25+ regulatory T-cells represent one major mechanism by which auto-reactive T-cells are controlled in the periphery. Deficiency in this cell population number or function could tilt the regulatory cell-pathogenic cell balance and lead to type-1 diabetes development. In this study, we describe a new method to expand antigen-specific CD4+ CD25+ regulatory T-cells from autoimmune-prone non-obese diabetic mice. CD4+ CD25+ regulatory T-cells were expanded in vivo using a combination of IL-2, anti-IL-2 antibody, BDC 2.5 peptide, and rapamycin. The expanded CD4+ CD25+ regulatory T-cells expressed a classical phenotype, displayed suppressive functions in vivo, and preliminary data suggest that these cells can delay diabetes development in NOD mice. This new method of peripheral tolerance induction could be used in humans to promote tolerance to islet cell transplants without relying on immunosuppressive drugs.
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