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Activation of T lymphocytes in the absence of a costimulatory signal can result in anergy or apoptotic cell death. Two molecules capable of providing a costimulatory signal, B7-1 (CD80) and B7-2 (CD86), have been shown to augment the immunogenicity of whole-tumor cell vaccines. To explore a potential role for costimulation in the design of recombinant anticancer vaccines, we used lacZ-transduced CT26 as an experimental tumor and beta-galactosidase (beta-gal) as the model tumor antigen. Attempts to augment the function of a recombinant vaccinia virus (rVV) expressing beta-gal by admixture with rVV expressing murine B7-1 were unsuccessful. However, a double recombinant vaccinia virus engineered to express both B7-1 and the model antigen beta-gal was capable of significantly reducing the number of pulmonary metastases when administered to mice bearing tumors established for 3 or 6 days. Most important, the double recombinant vaccinia virus prolonged the survival of tumor-bearing mice. These effects were antigen specific. The related costimulatory molecule B7-2 was found to have a similar, although less impressive enhancing effect on the function of a rVV expressing beta-gal. Thus, the addition of B7-1 and, to a lesser extent, B7-2 to a rVV encoding a model antigen significantly enhanced the therapeutic antitumor effects of these poxvirus-based, therapeutic anticancer vaccines.

Type

Journal article

Journal

Cancer research

Publication Date

06/1996

Volume

56

Pages

2832 - 2836

Addresses

Surgery Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.

Keywords

Animals, Mice, Inbred BALB C, Mice, Vaccinia virus, Lung Neoplasms, beta-Galactosidase, Membrane Glycoproteins, Vaccines, Synthetic, Antigens, CD, Viral Vaccines, Antigens, Neoplasm, Immunotherapy, Active, Survival Analysis, Female, B7-1 Antigen, B7-2 Antigen