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Mouse Melanoma Antigen Recognized by Lyt-2^- and L3T4^- Cytotoxic T-Lymphocytes¹

Department of Immunology, School of Medicine, Chiba University, Chiba, Japan 280 [K. O., K. T., T. I., Y. H., M. T.]; and Department of Biochemistry, Shizuoka College of Pharmacology, Shizuoka, Japan 422 [Y. H.]

A mouse melanoma (B16) antigen was investigated at a cellular level by three blocking experiments using monoclonal antimelanoma antibodies, soluble melanoma antigen, and enzyme-treated B16 melanoma cells as inhibitors. The activity of antimelanoma cytotoxic T-lymphocytes (CTL) was specifically reduced by addition of the mixture of two monoclonal antimelanoma antibodies, one (M2590) recognizing the cross-species melanoma epitope on G_M3(NeuAc) and the other (M562) reactive with the mouse melanoma-specific epitope on protein molecules. The CTL activity was also blocked by G_M3 liposome as well as by the soluble antigen. However, 3,000 times more G_M3 than the soluble melanoma antigen is required to obtain a similar inhibitory effect. When pronase-treated B16 melanoma cells, which have had protein molecules removed but G_M3 left intact on the surface, were used as an inhibitor, their blocking activity was greatly reduced but was still partly observed at a high inhibitor/target ratio. These results indicate that the melanoma antigen is not G_M3 itself but is composed of the G_M3-protein complex. This finding was also supported by using an interleukin 2-dependent CTL clone whose activity was blocked by both M562 and M2590. Antimelanoma CTL were found to belong to a double-negative T-cell population with Thy-1⁺, Lyt-2^-, L3T4^- phenotypes. L3T4⁺ T-cells were also demonstrated to be necessary for induction of double negative antimelanoma CTL.

¹ This work was supported by Grants-in-Aid for Cancer Research and for Scientific Research on Priority Areas from the Ministry of Education, Culture and Science, Japan, and also by the Princess Takamatsu Cancer Research Foundation and the Uehara Memorial Foundation.

² To whom requests for reprints should be addressed, at Department of Immunology, Chiba University, School of Medicine, 1-8-1 Inohana, Chiba, Japan 280.

Received 11/ 4/87. Revised 1/19/88. Accepted 2/19/88.