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Department of Neurosurgery, Medical School [T. Y., H. K., J. Y., H. H.], and Department of Pathology, Institute for Virus Research [S. K., M. T., Y. N., M. H.], Kyoto University, Kyoto 606, Japan
The effects of interleukin 2 (IL2) and interferon (IFN) on the generation and lytic activation of syngeneic murine malignant glioma (a methylcholanthrene-induced ependymoblastoma of C57BL/6 mouse origin, 203-glioma)-specific cytotoxic T-lymphocyte (G-CTL) were investigated. The surface marker analysis showed that G-CTLs from both intracranial and s.c. tumor-bearing mice were composed of thymectomy-resistant (mature) Lyt-1-.2.3+ and thymectomy-sensitive (immature) Lyt-1+.2.3+ CTLs, which markedly decreased concurrently with increased intracranial pressure. G-CTLs were confirmed to be activated with target specificity by both factors in a different way. The CTL activation by IL2 (20 units/ml) remained for a longer time, although a lag time of 5 days after initial culture was required. IL2 influenced Lyt-1+.2.3+ CTLs to proliferate and develop the lytic potential. In contrast, even a 3-h incubation with IFN (1000 units/ml) could enhance the cytotoxicity, but the augmenting effects were observed no longer than 5 days later. IFN activated Lyt-1-.2.3+ CTLs and increased their proportion of the total cell population with a simultaneous decrease of Lyt-1+.2.3+ CTLs. Therefore, it was suggested that IL2 may provide a grwoth of CTL populations and that IFN can accelerate recruitment of new effectors, causing activation of the lytic process.
1 Supported by grants from the Department of Neurosurgery, Kyoto University Medical School, Kyoto, Japan.
2 To whom requests for reprints should be addressed, at Department of Neurosurgery, Kyoto University Medical School, Shogoin, 54 Kawahara-cho, Sakyo-ku, Kyoto 606, Japan.
Received 7/ 7/86. Revised 1/20/87. Revised 11/10/87. Revised 2/12/88. Accepted 2/18/88.
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