SRC-SPECIFIC IMMUNITY IN INBRED CHICKENS BEARING V-SRC-DNA-INDUCED AND RSV-INDUCED TUMORS

The growth pattern (progression/regression) of v-src DNA- and Rous sar coma virus (RSV)-induced tumors was analogous on a panel of inbred chi cken lines. The decisive role of the major histocompatibility complex [Mhc(B)] alleles in resistance to the progression of these tumors was formally proved in segregating backcross populations. The immune mecha nism of tumor regression was demonstrated by both in vivo and in vitro assays. A protective effect of v-src-specific immunity against RSV ch allenge was shown in Rous sarcoma regressor line CB (B-12/B-12). Immun e cells from regressors of v-src DNA-induced tumors can protect syngen eic hosts from the development of tumor after challenge with both v-sr c DNA and RSV. Suppression of RSV-induced tumor cell growth in vitro w as also achieved by the use of cocultivation with spleen cells from ch ickens in which v-src DNA-induced tumors had regressed. This in vitro sarcoma-specific response was Mhc(B)-restricted. Chickens of the conge nic Rous sarcoma progressor line CC (B-4/B-4),e sometimes able to regr ess v-src DNA-induced tumors, but immune cells can only slow the growt h of v-src DNA-induced tumors in syngeneic hosts. This suggests that t he primary reason for the susceptibility of CC chickens is a weak v-sr c-specific immune response. Furthermore, some of the v-src DNA-induced tumors were transplantable across the Mhc(B) barrier The growth of tu mor allografts was able to be facilitated when immunological tolerance to the B-F/L region antigens (class I and class II) had been establis hed. This demonstrated that a high tumorigenicity of the transplantabl e tumor was not due to the lack of Mhc(B) antigens on tumor cells.