Article ViewAbstractThe Review of Diabetic Studies,2005,2,1,9-18.DOI:10.1900/RDS.2005.2.9Published:May 2005Type:Review Article Authors:David Thomas, Paola Zaccone, and Anne Cooke Author(s) affiliations:David Thomas, Paola Zaccone and Anne Cooke Department of Pathology, Immunology Division, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, United Kingdom. Abstract: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. Keywords:Dendritic cells, Foxp3, T cell, Treg cell, Type 1 diabetesView:PDF (455.4 KB) PDFClick here to download the PDF file. Images Regulation of islet inflammation ‹ Insulin-Producing Cells from Tissue Stem/Progenitor Cells: Are Autologous Cells Preferable to Allogeneic? up Proteomic Identification and Immunolocalization of Increased Renal Calbindin-D28k Expression in OVE26 Diabetic Mice ›