Cellular interactions modulating host resistance to tumours.

ABSTRACT

Active specific immunotherapy of carcinogen-induced rat tumours can be effected using vaccines containing tumour cells admixed with bacterial vaccines such as BCG and C. parvum. The nature of the tumour antigen preparation is important, the most effective immunogen being viable tumour cells whose growth is controlled by responses generated by the bacterial agent in the vaccine. Soluble tumour antigen preparations are usually ineffective due to the preferential induction of suppressor lymphocyte responses in normal hosts. In comparison, removal of suppressor precursors by cyclophosphamide treatment of animals leads to the development of tumour immunity following immunization with soluble antigen preparations. One component of the immune rejection response involves the generation of non-specific effector cells. This type of response can also be induced by administering chemical hypersensitizing agents so as to localize tumour deposits. This approach has proved highly effective in treating the guinea pig line 10 hepatoma by intralesional injection of alkylcatechols. These compounds are highly potent hypersensitizers, being the active constituents of the poison ivy/oak (urushiol oil), and localize in tumour cell membranes.