Characterization of macrophage recognition and killing of SV40- transformed tumor cells that are "resistant" or "susceptible" to contact-mediated killing

• Published in: The Journal of immunology (1950) Vol. 140; no. 2; pp. 589 - 596
• Main Authors: Chapes, SK, Duffin, D, Paulsen, AQ
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-01-1988; American Association of Immunologists
• Subjects: AKR murine leukemia virus - immunology; Animals; Biological and medical sciences; Cell Line, Transformed; Cell Transformation, Neoplastic - immunology; Cell Transformation, Viral; Cytotoxicity, Immunologic; Host-tumor relations. Immunology. Biological markers; Macrophage Activation; Macrophages - immunology; Medical sciences; Mice; Mice, Inbred C3H; murine leukemia virus; Phenotype; Simian virus 40 - immunology; Tumor Cells, Cultured - classification; Tumor Cells, Cultured - immunology; Tumor Virus Infections - immunology; Tumors; Transformed cell; Cytotoxicity; Chemical mediator; Activation; Papovaviridae; Host virus relation; Endogenous; Tumor cell; Binding; Oncovirinae; Cell-cell interaction; Polyomavirus; Rodentia; Retroviridae; Gene expression; Virus; Vertebrata; Cell contact; Mammalia; Cell line; Sensitivity resistance; Mouse; Oncogenic virus; Type C oncovirus; Murine leukemia virus; SV40 virus; Recognition; Macrophage
• DOI: 10.4049/jimmunol.140.2.589
• EISSN: 1550-6606
• ISSN: 0022-1767

In this report we used the macrophage-"resistant" and -"susceptible" cell lines, F5m and F5b, to determine why AKR or AKR-like virus expression makes the F5m cell line more resistant to in vitro macrophage killing than the F5b cell line. We found that resistance to macrophage killing may be transmitted by an infectious AKR or AKR-like murine leukemia virus and that resistance was concomitant with virus expression as measured by the presence of AKR virus-specific 70 kDa glycoprotein. We report that macrophage cytotoxicity of these cell lines is dependent upon the direct contact between tumor cells and macrophages. In contrast, macrophage-mediated cytostasis occurred via soluble macrophage products and no differential susceptibility of F5b or F5m to macrophage-mediated cytostasis was observed. Macrophage binding of F5b was also significantly better than that of F5m. These data suggest that only the events that depend upon the close contact of macrophages and tumor cells will be affected by the expression of AKR or AKR-like virus. Therefore, the differences in susceptibility of F5m and F5b to direct macrophage-mediated cytotoxicity are apparently because the macrophage binding of F5m is less efficient than the binding of F5b.