Augmentation of mouse natural killer activity and induction of interferon by tumor cells in vivo.

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Abstract
Conventional and nude mice inoculated with syngeneic or allogenic tumor cells developed a rapid rise in serum interferon (IF) levels, peaking within 24 h. Within the same period, natural killer (NK) activity was readily boosted in the spleen. Both activities usually declined at 3 days. Cells that lacked the ability to augment NK activity also failed to induce detectable levels of IF. The boosting of IF and NK functions did not appear to be a result of contamination of the tumor lines by viruses because inoculation of the several type C viruses into normal mice had no effect, and other viruses, like lymphocytic choriomeningitis virus and influenza, elevated IF and NK levels with a significantly later kinetics, peaking at 3-4 days. The IF induced by tumor cells was heat- and acid-labile, species-specific, and appeared to be in the type II class, although it was susceptible to antisera against Newcastle disease virus-induced IF. An early, nonthymus-dependent consequence of tumor-cell recognition is apparently the production of IF, which, in turn, activates NK cells to lyse the tumor cells.