Mice carrying the B cell leukemia (BCL1)+ were successfully treated by total lymphoid irradiation (TLI), cyclophosphamide, and allogeneic bone marrow (BM) transplantation. Long-term survivors were examined for residual BCL1 cells and for the ability to transfer adoptively graft vs. leukemia (GVL) activity. Residual BCL1 cells could not be detected in the allogeneic BM chimeras (> 14 to 16 months) with the use of indirect immunofluorescent staining with anti-idiotype antibody. However, residual tumor cells were present in 50% of the 'cured' chimeric mice since adoptive transfer of 106 spleen cells from 50% of the treated chimeric mice caused leukemia in BALB/c recipients. In order to determine whether leukemia had been prevented in the 'cured' chimeras by a persistent cell-mediated mechanism, BALB/c mice were injected with 106 spleen cells from the 'cured' BM chimeras together with a dose of 102 or 5 x 105 BCL1 cells. Onset of leukemia was delayed or completely abolished in a significant proportion of recipients receiving the cell mixtures, suggesting the presence of anti-tumor immunity in the cured mice. The data suggest that a persistent active immune mechanism may be responsible, in part, for the significant antileukemic effects observed in mice tolerant to donor alloantigens.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Immunology|
|Publication status||Published - 1983|
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