HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by La Motte, R. N. Articles by Mokyr, M. B. Search for Related Content PubMed PubMed Citation Articles by La Motte, R. N. Articles by Mokyr, M. B.

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.

This article has been cited by other articles:

				S. P. Murphy, R. Holtz, N. Lewandowski, T. B. Tomasi, and H. Fuji DNA Alkylating Agents Alleviate Silencing of Class II Transactivator Gene Expression in L1210 Lymphoma Cells J. Immunol., September 15, 2002; 169(6): 3085 - 3093. [Abstract] [Full Text] [PDF]

				A. Raiter, G. Rodionov, A. Novogrodsky, and B. Hardy CD4+ T lymphocytes as a primary cellular target for BAT mAb stimulation Int. Immunol., November 1, 2000; 12(11): 1623 - 1628. [Abstract] [Full Text] [PDF]

				Y. Zhan, A. J. Corbett, J. L. Brady, R. M. Sutherland, and A. M. Lew CD4 Help-Independent Induction of Cytotoxic CD8 Cells to Allogeneic P815 Tumor Cells Is Absolutely Dependent on Costimulation J. Immunol., October 1, 2000; 165(7): 3612 - 3619. [Abstract] [Full Text] [PDF]

				D. K. Sojka, M. Donepudi, J. A. Bluestone, and M. B. Mokyr Melphalan and Other Anticancer Modalities Up-Regulate B7-1 Gene Expression in Tumor Cells J. Immunol., June 15, 2000; 164(12): 6230 - 6236. [Abstract] [Full Text] [PDF]