Neoantigens and Microenvironment in Type 1 Diabetes: Lessons from Antitumor Immunity

Type 1 diabetes (T1D) is characterized by the selective and progressive destruction of insulin-producing beta cells by the immune system. An incomplete thymic selection against self-reactive islet antigens partly explains how these T cells reach the periphery and become diabetogenic. Increasing evidence suggest that beta cells themselves also participate to their own demise by generating neoepitopes that could be recognized by the immune surveillance machinery. In this regard, these T cells eradicate self-tissue by mechanisms analogous to a classical antitumor response. Cancer immunotherapy has exploited mutations and transcriptional and translational errors to trigger a specific antitumor response. In this opinion article, we aim at merging insight in antitumor immunology and autoimmunity to reveal processes that had previously been ignored to create beta cell-specific neoantigens.