Importance of B7-1-expressing host antigen-presenting cells for the eradication of B7-2 transfected P815 tumor cells

We have previously shown that B7-2 (CD86))-transfected P815 tumor cells eli cit tumor-eradicating immunity that leads to the regression of the B7-2(+) P815 tumor after transient growth in normal DBA/2 mice. Here, we show that both the B7-2 and B7-1 (CD80) molecules contribute to the eradication of B7 -2+ P815 tumors as treatment of the mice with both anti-B7-2 and anti-B7-1 mAb Mras required to prevent B7-2(+) P815 tumor regression. The cells that expressed the B7-1 molecule following inoculation of B7-2(+) P815 tumor cel ls into normal mice were not the tumor cells but rather host APCs including MAC-1(+) cells present in the draining lymph nodes. Moreover, B7-1-express ing host APCs were found to be important for the rejection of B7-2(+) P815 tumors as anti-B7-2 mAb alone, which was ineffective in preventing B7-2+ P8 15 tumor rejection by normal wild-type mice, was effective in preventing B7 -2+ P815 tumor rejection by mice in which the B7-1 gene was disrupted. Fina lly, consistent with the importance of B7-1-expressing host APCs for the ge neration of tumor-eradicating immunity against b7-2(+) P815 tumor cells, CD 4(+) T cells (not only CD8(+) T cells) were found to participate in tumor-e radicating immunity against B7-2+ P815 tumor cells. Thus, in addition to el iciting tumor-eradicating immunity directly, B7-2(+) P815 tumor cells elici t tumor-eradicating immunity indirectly through B7-1-expressing host APCs t hat present tumor-associated Ags to CD4(+) T cells.