Failure to detect anti-group-specific murine leukemia virus activity in tetraparental AKR-CBA chimeras.

Tetraparental AKR-CBA/H-T6 chimeras were primarily derived and investigated to determine whether factors associated with the tumor resistance of the CBA/H-T6 could overcome the innate lymphoma susceptibility of the AKR. Evidence has since shown that, on comparison with the AKR, lymphomas were not only delayed but were also less common in a group of 18 early embryo aggregation derived AKR-CBA/H-T6 tetraparental chimeras. Evidence here has shown other clear differences between the AKR and AKR-CBA/H-T6 chimeras. Whereas murine group-specific murine leukemia viral antigens were detected in the sera in both situations, immunoabsorption studies showed that, in the AKR, the antigens exist complexed to the corresponding antibodies. The situation in the chimeras was in complete contrast, since here antigens exist as a "free" form. This in turn has led us to suggest that the advantage in respect to tumor immunity in the AKR-CBA/H-T6 chimeras is due to the tolerance to oncogenic virus being maintained. In this situation and in contrast to the AKR, in the absence of "masking" antibody-viral antigenic complexes, "normal" tumor immunity can be effected. It has to be assumed that tolerance to the oncogenic Gross virus in the AKR-CBA/H-T6 chimeras reflects the influence of the CBA component. How this has possibly been achieved is discussed.