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Mounting evidence indicates the beta-cell is more than just a passive target in the development of T1D: the lack of long-term success with immune intervention therapies, the existence of islet autoimmunity without T1D development, and the persistence of beta-cells after diagnosis and T1D progression, all provide evidence that the beta-cell is an active participant along with the immune system in T1D pathogenesis (6, 7)

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