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Regulatory T Cells Prevent Transfer of Type 1 Diabetes in NOD Mice Only When Their Antigen Is Present In Vivo¹

Department of Immunology, University of Colorado at Denver and National Jewish Medical and Research Center, Denver, CO 80206

Regulatory T cells (Tregs) can potentially be used as tools to suppress pathogenic T cells in autoimmune diseases such as type 1 diabetes. For use in therapy it is critically important to determine whether suppression by Tregs requires a population specific for the target of autoimmunity, such as pancreatic β cells in type 1 diabetes. Current reports in the NOD mouse model of type 1 diabetes are in conflict as to whether suppression of disease by Tregs is Ag-dependent. We have addressed this question by evaluating the effects of islet-specific TGF-β-induced Tregs in recipient mice in which the Treg Ag is either present or absent. Our data show that Treg numbers in pancreas are reduced in the absence of Ag and that there are Ag-dependent differences in the effects of Tregs on pathogenic T cells in the pancreas. By examining protection from diabetes induced by T cell transfer, we have clearly demonstrated that Tregs suppress only in the presence of their Ag and not in mice in which the islets lack the Treg Ag. Our results also suggest that in sufficiently large populations of polyclonal Tregs, there will be adequate numbers of islet-specific Tregs to suppress diabetes.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by research grants from the Juvenile Diabetes Research Foundation (JDRF 1-2004-49) and the National Institutes of Health (RO1 DK50561).

² Address correspondence and reprint requests to Dr. Kathryn Haskins, Department of Immunology, University of Colorado at Denver, 1400 Jackson Street, NJMRC K823, Denver, CO 80206. E-mail address: katie.haskins{at}uchsc.edu

³ Abbreviations used in this paper: Treg, regulatory T cell; TCR-Tg, TCR transgenic.