Importance of interferon α in the resistance of allogeneic C57B1/6 mice to the multiplication of friend erythroleukemia cells in the liver

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Abstract
Friend erythroleukemia cells (FLC) (H‐2d) injected intravenously multiply extensively in the livers of syngeneic DBA/2 mice and not at all in the livers of allogeneic C57B1/6 mice. Our results indicate that interferon α (IFN‐α) is an important factor in the resistance of allogeneic mice to the multiplication of FLC in the liver. (a) After i.v. inoculation of FLC there was an inverse correlation between the presence of IFN‐α in the serum and the capacity of FLC to multiply in the liver. Thus, all 44 FLC‐injected adult C57B1/6 mice had circulating IFN‐α and FLC did not multiply in the liver of any of the mice. Interferon was not detected in the serum of 83% of 41 FLCinjected DBA/2 mice (and was found only at a low titer in 17% of the mice) and FLC multiplied in the liver of all mice. (b) FLC did multiply in the livers of newborn C57B1/6 mice and in the livers of irradiated adult C57B1/6 mice, and IFN‐α was not detected in their sera. In contrast, after i.v. inoculation of FLC, IFN‐α was detected in the sera of 3‐week‐old and athymic nu/nu adult C57B1/6 mice while FLC failed to multiply in the liver. (c) FLC also induced IFN‐α in congenic B10.D2 (H‐2d) mice and FLC did not multiply in the liver. We suggest that, depending on the site of tumor implantation, different host mechanisms have various degrees of importance in controlling the growth and/or rejection of allogeneic tumor cells, and that IFN‐α is particularly important when FLC are injected i.v.

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