Interferon treatment of murine meth‐a sarcoma cells: Effects on the malignant phenotype and expression of tumor‐specific and H‐2 antigens

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Abstract
A virus‐free methycholanthrene‐induced sarcoma (Meth‐A) in BALB/c mice was grown in culture and treated with purified mouse interferon (α and β mixture) prior to testing for oncogenicity in the host animal. Use of interferon in vitro caused growth inhibition, but not cytotoxic effects; such effects were fully reversible upon interferon removal from the system. There was a significant decrease in tumor incidence in mice challenged with interferon‐treated cells, but this could be overcome by sufficiently increasing the number of cells in the inoculating dose. By transplanting these BALB/c sarcoma cells into Sprague‐Dawley nude mice, the effects of interferon could be negated. Since these mice have an unaltered activity of NK cells, the results suggest that NK cells do not play a major role in rejection of the Meth‐A tumor, but that the reduction in tumor incidence is dependent on the presence of functional T cells. Interferon caused a detectable reduction in the expression of the tumor‐specific transplantation antigen (TSTA) associated with Meth‐A cells, but increased the expression of H‐2 antigens. It has recently been shown that H‐2 antigens play a role in host recognition of the TSTA of methylcholanthrene‐induced sarcomas. It is suggested that the increased expression of H‐2 antigens on interferon‐treated Meth‐A cells could lead to an increased frequency of recognition by T‐cells.

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