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Type 1 diabetes is a T cell-mediated autoimmune disease that is characterized by Ag-specific targeting and destruction of insulin-producing β cells. Although multiple studies have characterized the pathogenic potential of β cell-specific T cells, we have limited mechanistic insight into self-reactive autoimmune T cell development and their escape from negative selection in the thymus. In this study, we demonstrate that ectopic expression of insulin epitope B:9-23 (InsB 9-23 ) by thymic APCs is insufficient to induce deletion of high- or low-affinity InsB 9-23 -reactive CD4 + T cells; however, we observe an increase in the proportion and number of thymic and peripheral Foxp3 + regulatory T cells. In contrast, the MHC stable insulin mimetope (InsB 9-23 R22E) efficiently deletes insulin-specific T cells and prevents escape of high-affinity thymocytes. Collectively, these results suggest that Ag dose and peptide-MHC complex stability can lead to multiple fates of insulin-reactive CD4 + T cell development and autoimmune disease outcome.

Ectopic Expression of Self-Antigen Drives Regulatory T Cell Development and Not Deletion of Autoimmune T Cells