Failure to detect antibody against Gross virus in tetraparental AKR ↔ CBA mouse chimaeras

Abstract

In spite of early acquisition upon the germ line, tolerance to the Gross (gs) virus is short-lived in the AKR. From about the age of 3 months anti-gs antibodies occur and these complex with the corresponding viral antigens. Such complexes are best seen in the glomeruli by means of immunofluorescence. In marked contrast to the AKR, renal complexes were minimal in a group of AKR reversible CBA/H-T6 chimaeras derived by early embryo aggregation. This was particularly surprising since large numbers of type C murine leukaemia virus-like particles were identified in the chimaeras and the tissues were found to be saturated with gs antigen. The lack of renal antigen-antibody complexes was the first suggestion that anti-gs antibody might not be present in the chimaeras and renal elution studies here support this assumption. In contrast to the AKR where "split " renal eluates have been shown to have anti-gs activity, no activity was demonstrated in eluates from any of the chimaras. Tolerance to the oncogenic Gross virus in the chimaeras has to be attributed to the CBA parental strain component and since this component is also held responsible for the tumour resistance of these chimaeras, both phenomena could well be related. In this context it would appear that in the absence of masking by antibody viral antigenic complexes, tumour specific sites can be recognized in the chimaeras and unlike the AKR "normal" tumour immunity can be effected. This hypothesis is currently bei-ng tested.