| Rev Diabet Stud, 2005, 2(1):9-18 | DOI 10.1900/RDS.2005.2.9 |
David Thomas, Paola Zaccone, Anne Cooke
Department of Pathology, Immunology Division, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, United Kingdom.Keywords: type 1 diabetes, T cell, Treg cell, Foxp3, dendritic cells
Type I diabetes is increasing in incidence in developed countries [1]. Diabetes arises from a breakdown of tolerance to islet antigens, resulting in T cell-driven destruction of the islet cells and concomitant hyperglycemia. In this review, we explore whether this loss of tolerance results in part from a defect in the action of regulatory T cells. We draw on both human data and that obtained from NOD mice, the murine model of autoimmune diabetes. Although insulin-based therapies have been highly successful in treating diabetes, the complications of long-term hyperglycemia are still major causes of morbidity and mortality. Accordingly, we also discuss whether treatment with regulatory T cells is a viable method for restoring long-term tolerance to self-antigens in recently diagnosed or pre-diabetic individuals. Regulatory T cell therapy offers many potential advantages, including a specific and lasting dampening of inflammation. However, some significant hurdles would have to be overcome before it could become an established treatment.
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