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Deleting islet autoimmunity

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Abstract

Even though there are numerous autoantigens for type 1 diabetes, current evidence suggests that a single autoantigen, namely insulin, is responsible for the key initiating event in autoimmunity. If a single autoantigen is necessary for triggering the autoimmune process, then antigen-specific therapy to block or delete the immune response against that autoantigen before epitope spreading occurs, may become a larger focus of future immunotherapeutic strategies. In this article, we review current literature regarding insulin as an autoantigen and potential approaches to deleting insulin-reactive T cells through the use of peptide vaccines and targeted T cell receptor immunizations.

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Acknowledgments

Research supported by NIH (R01 DK32083, DK32493, DK 55969, DK 06218, DK06405); Immune Tolerance Network (AI 15416); Diabetes Endocrine Research Center (DK 057516); Autoimmunity Prevention Center (AI 50864); and Clinical Research Centers Program (M01 RR00069, M01RR00051), American Diabetes Foundation, Juvenile Diabetes Foundation, and the Children’s Diabetes Foundation.

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Correspondence to George S. Eisenbarth.

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Liu, E., Li, M., Jasinski, J. et al. Deleting islet autoimmunity. Cell Biochem Biophys 48, 177–182 (2007). https://doi.org/10.1007/s12013-007-0022-9

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