In summary, we presented two main new findings: (1) changing the structural integrity of the vector-encoded ppins protein affected the priming of effector CD8+ T cells in an epitope-specific manner; and (2) changing the natural expression of ppins in the ER prevented priming of ppins-specific CD8+ T cells, suppressed the potential multi-specific immune response against beta cell antigens, and protected NOD mice from diabetes development. The gene discussed is CD8A; the disease is diabetes mellitus.