Host B7-1 and B7-2 costimulatory molecules contribute to the eradication of B7-1-transfected P815 tumor cells via a CD8(+) T cell-dependent mechanism

B7-1 (CD80)-transfected P815 tumor cells were previously shown to elicit tu mor-eradicating immunity that leads to the regression of B7-1(+) P815 tumor s after transient growth in normal syngeneic (DBA/2) mice. Here, we show th at not only the B7-1 molecule but also the B7-2 (CD86) molecule contributed to the eradication of B7-1(+) P815 tumors. The B7-1 molecule that contribu ted to the eradication of B7-1(+) P815 tumors was expressed not only on the tumor cells but also on host APCs, including MAC-1(+) cells. The B7-2 mole cule that contributed to the eradication of B7-1(+) P815 tumors was express ed only on host APCs, such as B220(+) cells, and not on the tumor cells, Zn spite of the fact that B7-expressing host APCs contributed to the eradicat ion of B7-1(+) P815 tumors, only CD8(+) T cells without help from CD4(+) T cells were important for tumor eradication. Taken together, these findings indicate that in addition to the ability of B7-1-transfected tumor cells to stimulate CD8(+) T cell-mediated tumor-eradicating immunity directly, such tumor cells can also stimulate CD8(+) T cell-mediated tumor-eradicating im munity indirectly as a result of cross-priming through B7-expressing host A PCs.