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Importance of B7-1-Expressing Host Antigen-Presenting Cells for the Eradication of B7-2 Transfected P815 Tumor Cells¹

Ross N. La Motte^2,*, Arlene H. Sharpe, Jeffrey A. Bluestone^3, and Margalit B. Mokyr^3,4,*

^* Department of Biochemistry and Molecular Biology, University of Illinois at Chicago, Chicago, IL 60612; Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115; and The Ben May Institute for Cancer Research, the Committee on Immunology, and the Department of Pathology, University of Chicago, Chicago, IL 60637

We have previously shown that B7-2 (CD86)-transfected P815 tumor cells elicit 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 was required to prevent B7-2⁺ P815 tumor regression. The cells that expressed the B7-1 molecule following inoculation of B7-2⁺ P815 tumor cells 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-expressing 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⁺ P815 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. Finally, consistent with the importance of B7-1-expressing host APCs for the generation of tumor-eradicating immunity against B7-2⁺ P815 tumor cells, CD4⁺ T cells (not only CD8⁺ T cells) were found to participate in tumor-eradicating immunity against B7-2⁺ P815 tumor cells. Thus, in addition to eliciting tumor-eradicating immunity directly, B7-2⁺ P815 tumor cells elicit tumor-eradicating immunity indirectly through B7-1-expressing host APCs that present tumor-associated Ags to CD4⁺ T cells.

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