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B7-1 Expression by a Non-Antigen Presenting Cell-derived Tumor

Sections of Immunobiology [S. J. A.], Medical Oncology [T. M-A.], and Immunobiology [G. S.], Yale School of Medicine, and Howard Hughes Medical Institute, Section of Immunobiology [J. M., R. A. F.], Yale School of Medicine, New Haven, Connecticut 06510

The existence of a naturally occurring immunosurveillance against neoplastic cells is controversial. A difficulty with this concept is that tumor-specific antigen-reactive T cells would not be expected to become activated after encountering tumor cells, since T cells that bind to antigen in the absence of the costimulation provided by antigen-presenting cells may be inactivated. We studied a transgenic model of tumorigenesis where T cells reactive to a particular tumor-specific antigen are lost prior to the development of non-antigen-presenting cell-derived tumors; therefore, the tumors that develop are not subjected to immunosurveillance. We found that a tumor cell line derived from one such tumor expresses the T-cell costimulatory molecule B7-1, the expression of which is normally restricted to antigen-presenting cells. In addition, we found that several immortalized cell lines, which are nontumorigenic and thus have suffered only early genetic events in the tumorigenesis process, express B7. This suggests that a host cell can be induced to express surface B7-1 molecules after suffering an oncogenic insult, which might possibly be a primary mechanism of immunosurveillance against tumors.

¹ Present address: Division of Medical Oncology and Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612.

² R. A. F. is an Investigator of the Howard Hughes Medical Institute.

³ To whom requests for reprints should be addressed, at Howard Hughes Medical Institute, Research Laboratory, Yale University, Section of Immunobiology, 310 Cedar Street, FMB 412, New Haven, CT 06510.

Received 2/21/95. Accepted 4/21/95.

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