Immunogenicity is the ability of antigens to elicit an immune response. The host immunity for anti-tumor can be induced because of the existence of tumor-specific and/or tumor-associated antigens. However, the most effective immune manipulation for ovarian carcinoma is eagerly awaited. To explore the systemically and locally kinetic changes of immunologic profiles during tumor progression and to elucidate the inhibition of tumor growth and the reverse of immunologic profiles by depletion of Treg cells in ovarian carcinomas, ovarian cancer patients and the ascitogenic animal model were employed. Immunologic profiles with flow cytometric analyses, immunohistochemistric staining, RT-PCR, ELISA, and ELISPOT assays were performed. In vivo depletion of Treg cells with the mAb PC61was also performed in the animal model. Including the anti-inflammatory cytokines IL-4 and TNF-α significantly decreased, TGF-β, IL-6, IL-10 significantly elevated in human ascites when the disease progressed to advanced diseases. The ratios of CD8+ T cell/Treg cell in the tumor asociated lymphocytes of the human ascites were lower in advanced diseases than those in early diseases. These alterations of immune components during tumor progression were proved in our animal model. Mice, when treated with kinetic low dose of mAb PC61, showed longer survival than the other groups. Tumor-bearing mice treated with kinetic low dose mAb PC61could inhibit the suppressive immunologic profiles, enhance the effective immunologic profiles, and generate potent antigen-specific anti-tumor immunities and effects. We concluded that the imbalance between effective and suppressive immunities could be identified in tumor-bearing situation, especially in advanced diseases. The depletion of Treg cells could correct the immunologic profiles and generate potent antigen-specific immunity. The strategy of targeting Treg cells can be a new strategy for the immunotherapy of ovarian carcinoma.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3536. doi:1538-7445.AM2012-3536