Inhibition of transplanted sarcomas mediated by BCG in rats with a defined immunological deficit.

Experiments were undertaken to test the hypothesis that a major component of BCG contact-induced inhibition of syngeneic tumour growth in rats is not dependent on the participation of thymus-processed (T) cells. Hosts were deprived of T cells by thymectomy followed by either lethal irradiation (850 rad) and bone marrow reconstitution, or repeated whole body irradiation to a total dose of 1,000 rad. After 6 weeks had elapsed to allow for bone marrow restitution, rats were challenged with trypsinized sarcoma cells admixed with Glaxo strain BCG. For sarcoma P7, host T-cell deprivation did not significantly diminish the capacity of BCG to prevent the progressive development of this neoplasm from an inoculum of one million cells. Under similar conditions, the incidence of sarcoma CC5 development in maximally deprived hosts was significantly greater (7/19) than in normal controls (1/16) (P is less than 0.05), but the majority of rats (58%) did not succomb to tumour outgrowth. In the case of a third neoplasm--a spontaneously metastasizing fibrosarcoma (P8)--the effect of BCG on primary tumour development was comparable in normal and deprived recipients and was limited to temporary arrest as distinct from complete inhibition. Assessment of the influence of BCG on lung metastases was more complex since the extent of metastatic disease from subcutaneous tumour cells alone was greater in deprived rats than in normal rats. It is concluded that T-cell participation is not a major requirement for BCG contact-induced inhibition in this system and some implications for the mechanism of action are discussed.