Abstract
In this report, we demonstrate that B7-H1, a B7 family molecule implicated in tumor immune evasion, is constitutively expressed on 66% of freshly isolated squamous cell carcinomas of the head and neck (SCCHN). To define the potential impact of tumor-associated B7-H1 on immunotherapy, the B7-H1-negative mouse SCC line, SCCVII, was transfected to express B7-H1. Although all of the animals succumbed to B7-H1/SCCVII tumors even after adoptive T-cell immunotherapy, the infusion of B7-H1 blocking monoclonal antibody with activated T cells cured 60% of animals. These data support B7-H1 blockade as a new approach to enhance the efficacy of T-cell immunotherapy.
Footnotes
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The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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↵1 Supported by NIH Grants DE00459 and CA97085, and by Mayo Foundation.
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↵2 S. E. S. and H. D. contributed equally to this article.
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↵3 To whom requests for reprints should be addressed, at Mayo Clinic, Department of Otolaryngology, 200 First Street SW, Rochester, MN 55905. Phone: (507) 284-3853; Fax: (507) 284-8855; E-mail: strome.scott{at}mayo.edu
- Received April 15, 2003.
- Revision received June 25, 2003.
- Accepted July 8, 2003.
- ©2003 American Association for Cancer Research.
Volume 63, Issue 19
