The development of diabetes in NOD mice is a T-cell-dependent autoimmune phenomenon. To clarify which subset of T cells is responsible for the destruction of B cells in islets of NOD mice, we injected precritical NOD mice (12 weeks old) with monoclonal antibodies (anti-L3T4 mAb and anti-Ly-2 mAb), which react with mouse lymphocytes. The administration of anti-L3T4 mAb prevented diabetes in the NOD mice, while anti-Ly-2 mAb failed to do so. Histologically, severe insulitis similar to that in the control mice was observed in both anti-L3T4 mAb-and anti-Ly-2 mAb-trea ted mice. However, the subsets of T cells constructing insulitis were entirely different in the two groups. Ly-2-positive T cells were dominant, while L3T4-positive T cells were absent, in the islets of anti-L3T4 mAb-treated mice. In the anti-Ly-2 mAb-treated group, most of the infiltrated lymphocytes were L3T4-positive T cells, and no Ly-2-positive T cells were observed.
These results lead to the conclusion that L3T4-positive T cells may play a major role not only in the development of insulitis but in the destruction of B cells in NOD mice.
