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The results demonstrated that stimulation of animals with TAP and MHC-I proficient tumor cells generated antigen specific T cells with greater killing activities than those of TAP and MHC-I deficient tumor cells.
Next, we performed in vitro and in vivo experiments to determine whether the TAP and MHC-I proficient CMT.TAP1,2/Kb was able to induce tumor-antigen specific immunity.
This discrepancy was traced to differences in the ability of dendritic cells (DCs) to access and sample different antigen reservoirs in TAP and MHC-I proficient versus deficient cells and thereby stimulate adaptive immune responses through the process of cross-presentation.
A conflicting report exists from Huang et al [15] who used the MHC-I negative B78H1 and its MHC-I proficient transfectant (derived from B16 melanoma) as a model system to immunize mice and then challenged with MHC-I positive B78H1 cells.
These results provide an explanation why immunization with MHC-I proficient (CMT.TAP1,2/Kb) cells can increase the generation and production of T cells resulting in immune responses greater than those adaptive T cell responses generated by immunization with MHC-I deficient (CMT.64) cells.
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