Sendai Virus Infection of Tumor Cells Increases the Production of Autoreactive H-2 Specific Antibodies in Syngeneic Recipients
The major histocompatibility complex (MHC) phenotype of neoplastic cells reflects both the cells tumorigenic history and its internal state of differentiation and metabolic activity. In many cases MHC expression probably also affects the outcome of the disease. An increasing body of evidence indicates that various agents are able to increase the immunogenicity of malignant cells. An increase in the immunogenicity of tumor cells was observed following in vitro treatment with various drugs (Koyama and Ishii 1969; Tsukagoshi and Hashimoto 1973; Frost et al. 1983; Carlow et al. 1985; Gorelik et al. 1985; Flood et al. 1987), UV light treatment (Peppoloni et al. 1985), and virus infection (Wakamiya et al. 1986; Williams et al. 1986) of tumor cells. Recently, we have shown (Opolski et al. 1987) that the median survival time of mice inoculated with Sendai virus-infected EL4 tumor cells was significantly longer (in some animals a complete rejection was observed) than in those inoculated with untreated EL4 cells. Moreover, most of the mice which rejected Sendai virus-infected EL4 cells were found to be resistant to subsequent inoculation of untreated EL4 tumor cells (Opolski et al. 1987). What remains unknown is which of the changes on the cell surface are responsible for the conversion of the weakly or nonimmunogenic tumor cells into a highly immunogenic form. Numerous experimental data indicate that cell surface antigens are recognized by T-Iymphocytes in association with MHC products (Zinkernagel and Doherty 1975). One might postulate that conversion of nonimmunogenic tumor cells into a highly imunogenic form would be paralleled by changes in expression of MHC products on the surface of tumor cells (Goodenow et al. 1985).
KeywordsMajor Histocompatibility Complex Sendai Virus Lewis Lung Carcinoma Tumor Syngeneic Recipient Sendai Virus Infection
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