Hans Olof Sjögren

Summary Host resistance against methylcholanthrene (MC)-induced sarcomas, demonstrated by previous authors after transplantation to isologous recipients, could also be shown to occur in the primary autochthonous host, whose tumor had been operatively removed. The autochthonous mice, together with groups of isologous animals, were pretreated with irradiated sarcoma cells and subsequently challenged with increasing doses of viable cells, also inoculated into untreated isologous controls. An increased resistance could be demonstrated with twelve out of sixteen tumors in the autochthonous and nineteen out of 22 tumors in the isologous host. Resistance was relative rather than absolute and broke down when the dose of viable cells was progressively increased. It was usually stronger in isologous than in autochthonous mice, but this was not a general rule. Isologous mice pretreated with irradiated normal tissues and subsequently challenged with viable sarcoma cells showed either no increase in resistance or a slight increase that exceeded the control level but did not reach the level found in isologous hosts pretreated with irradiated cells of the same sarcoma. Isologous, untreated mice that had received total-body irradiation before being challenged with viable sarcoma cells supported the growth of small viable inocula better than did unirradiated isologous hosts. In the cases tested, resistance against a given sarcoma did not lead to cross-resistance against a different sarcoma, induced in the same genotype by MC. Serial treatment with homologous, MC-induced sarcoma tissue did not reduce the yield of primary sarcomas obtained after application of MC. Lymph node cells, but not serum, of isologous mice pretreated with heavily irradiated sarcoma cells, could neutralize the sarcoma cells wholly or partially upon incubation in vitro. Lymph node cells of untreated animals and preimmunized lymph node cells killed by freezing and thawing had no effect.

Summary Fifty-two polyoma-induced primary mouse tumors were tested for transplantability in isologous recipients. Thirty-five tumors grew progressively in the subcutaneous tissue, and several lines have been established in serial transplantation. The remaining tumors did not grow out at all upon transfer. Eleven among the transplantable tumors have been tested by inoculating known numbers of cells to the following three groups of adult isologous recipients: ( a ) untreated mice, maintained at a separate, polyoma-free colony, ( b ) mice preimmunized as adults against polyoma virus containing supernatant fluids from infected mouse embryo tissue cultures, and ( c ) mice pretreated with heavily irradiated cells of the same tumor. There was a clear and consistent difference between groups a and b for ten of eleven tumors, indicating a state of resistance against transplantation of the established polyoma tumors in the virus-immunized group. With the exception of two out of nine experiments, there was no evidence of resistance in group c , pretreated with irradiated tumor cells. Serum of virus-immunized mice had a certain inhibiting effect on viable polyoma tumor cells upon incubation in vitro with one of four tumors. The possible implications of these findings have been discussed.

Summary It was found that a state of relative resistance can be built up in highly inbred skin-compatible C3H mice against the isotransplantation of lymphomas recently induced in the same strain by the Gross virus. Resistance could be built up in two different ways: by pretreating the recipients with homografts of other Gross lymphomas, induced in genetically incompatible mice, or with sub-threshold doses of cells from the same isologous lymphoma. The resistance was relatively weak in comparison with the previously demonstrated antigenicity of methylcholanthrene-induced sarcomas and polyoma-induced tumors. There appears to be partial or complete cross-resistance between different lymphomas induced by the Gross virus.

Mouse sarcoma cells derived from recent methylcholanthrene-induced tumors of known genotypes were inoculated into isologous or homologous hosts after incubation with serum or lymph node cells from different sources. Isoantiserum enhanced the outgrowth of the tumors in genetically incompatible, homologous systems, whereas in isologous systems it had no effect. Lymph node cells of preimmunized homologous hosts were inhibitory in both homologous and isologous systems. Homologous lymph node cells, taken from untreated mice, showed variable effects, depending on the system used. Based on this experience, obtained with various experimental designs, all of which were concerned with some aspect of the homograft reaction, similar studies were carried out with completely isologous systems. Primary or first or second passage sarcomas were exposed to lymph node cells of isologous mice, pretreated with heavily irradiated cells of the same tumor, or of the primary autologous host. Lymph node cells derived from autologous, or untreated or pretreated isologous, hosts were inhibitory in a number of cases.