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Type 1 diabetes can be inhibited in standard NOD mice by autoantigen-specific immunotherapy targeting pathogenic CD8+ T-cells. NOD.β2m(null).HHD mice expressing human HLA-A2.1 but lacking murine major histocompatibility complex class I molecules develop diabetes characterized by CD8 T-cells recognizing certain autoantigenic peptides also targeted in human patients. These include peptides derived from the pancreatic β-cell proteins insulin (INS1/2 A(2-10) and INS1 B(5-14)) and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP(265-273) and IGRP(228-236)). Hence, NOD.β2m(null).HHD mice represent a model system for developing potentially clinically translatable interventions for suppressing diabetogenic HLA-A2.1-restricted T-cell responses.

Prevention of “Humanized” Diabetogenic CD8 T-Cell Responses in HLA-Transgenic NOD Mice by a Multipeptide Coupled-Cell Approach