The development and specific suppression of concomitant immunity in two syngeneic tumour‐host systems

Immunological resistance, concomitant with tumour growth, against two methyl‐cholanthrene‐induced murine sarcomas MC23 and MC6 differing widely in their immunogenicities, was studied in inbred C57BL and BALB/c strains of mice which are syngeneic with the respective tumours. It was found that, initially, immune responses to specific transplantation antigens resulted in a peak of antitumour resistance at 10–14 days after the implantation of the tumours. In the second phase of tumour growth a rapid decline of the resistance was observed. The peak at 10–14 days was followed by a greater than 50% loss of resistance to re‐inoculation with the tumour cells, 1 week later. Further decline of resistance in the MC6‐BALB/c system was followed by the acceptance and progressive growth of over‐threshold doses of tumour cells. A comparable observation could not be made in the immunogenically weaker MC23‐C57BL system where further loss of resistance was gradual. The above changes in the development and decline of anti‐tumour resistance were broadly correlated with the progress of the immunoblast reaction of the paracortical areas of regional lymph nodes. Changes of anti‐tumour resistance in the MC6‐BALB/c system were found to be associated with corresponding changes in the availability and/or effectiveness of specifically cytotoxic lymphoid cells, in the lymphoid organs, as well as a change in the quality of the serum factors from weakly inhibitory to mildly enhancing, in the tumour. Specifically cytotoxic lymphoid cells could not be demonstrated in the MC23‐C57BL system by the lymphocyte neutralization technique employed, possibly due to the involvement of in vivo blocking phenomena. Accordingly, sera of these mice proved to be tumour‐enhancing throughout the period of tumour growth. It is suggested that the progressive growth of the tumours is facilitated by the specific suppression of cell‐mediated immunity by the “efferent” as well as by the “afferent” mechanisms and is brought about by a factor or factors–possibly antibody and/or antigen‐antibody complexes–present in the serum of the tumour‐bearing mice.