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Decreased Susceptibility of Lined Human Gliosarcoma Cells to Lymphokine-activated Killer Cell Cytolysis by -Interferon Treatment¹

Department of Neurosurgery, Faculty of Medicine [S-I. M., H. K., Y. O., T. N., J. T., S. K., M. M., T. Y., K-I. I., T. A.], and Department of Pathology [Y. N.], Institute for Virus Research, Kyoto University, Kyoto, and Department of Clinical Pathology, Kobe City General Hospital, Kobe [S. K.], Japan

The susceptibility of the established cultured gliosarcoma line GI-1 to lymphokine-activated killer (LAK) cells was analyzed with and without interferon (IFN)- treatment of target GI-1 cells. IFN- treatment decreased the susceptibility of GI-1 cells to LAK cell cytolysis in a dose-dependent manner. Acid treatment of GI-1 cells increased their susceptibility to cytolysis compared with untreated cells. IFN- treatment and acid treatment of GI-1 cells respectively increased and decreased the expression of class I HLA antigens on GI-1 cells. The susceptibility of GI-1 cells to LAK cell cytolysis and their expression of HLA class I molecules were inversely correlated. Subpopulation depletion experiments on the LAK cells with monoclonal antibodies and complement revealed that phenotypically natural killer type (CD16+) cells had a high cytotoxic activity against untreated GI-1 cells but a relatively low activity against IFN--treated GI-1 cells in both the precursor and effector phases. On the other hand, phenotypically T-type (CD3+) cells did not show these tendencies at all in both the precursor and the effector phases.

¹ This work was supported in part by a Grant-in Aid for Cancer Research (63-17) from the Ministry of Health and Welfare of Japan.

² To whom requests for reprints should be addressed, at Department of Neurosurgery, Faculty of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ko, Kyoto 606, Japan.

Received 7/18/89. Revised 10/11/89. Accepted 10/30/89.