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Response to Comment on: Tritt et al. (2007) Functional Waning of Naturally Occurring CD4⁺ Regulatory T-Cells Contributes to the Onset of Autoimmune Diabetes: Diabetes 57:113–123, 2007

From the Department of Microbiology and Immunology and McGill Center for the Study of Host Resistance, McGill University, Montreal, Quebec, Canada, H3A 2B4

Address correspondence and reprint requests to Dr. Ciriaco A. Piccirillo, Department of Microbiology and Immunology, McGill University, 3775 University St., Room 510, Lyman Duff Medical Building, Montreal, QC, Canada, H3A 2B4. E-mail: ciro.piccirillo@mcgill.ca

The first 20% of the full text of this article appears below.

We thank Thomas et al. (1) for their insightful comments regarding the functional dynamics of CD4⁺Foxp3⁺ regulatory T-cells (Tregs) in their model of type 1 diabetes. An impressive array of studies in the literature establishes that CD4⁺Foxp3⁺ Tregs play a central, master-switch role in peripheral tolerance in the NOD mouse model of spontaneous type 1 diabetes (2,3). A central question is whether the onset of spontaneous disease in NOD mice results from a decline in regulation over time or from uncontrollable activity of self-reactive T-cells. Type 1 diabetes may reflect subtle, functional deficiencies in regulatory T-cells, thus allowing the diabetogenic process to unfold. In our study (4), we attempted to determine whether temporal, quantitative, or qualitative defects in CD4⁺Foxp3⁺ Tregs contribute to spontaneous type 1 diabetes.

The BDC2.5 mouse model contains a highly pathogenic CD4⁺ T-cell repertoire and represents a . . . [Full Text of this Article]

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