Regulation of the immune response to tumor antigen
Abstract
Reduction of syngeneic tumor growth in primary tumor-bearing murine hosts has been accomplished using a variety of treatments designed to decrease endogenous suppressor cell activity or augment host effector responses. Selective interference with suppressor cell function can be achieved by in vivo administration of anti-thymocyte serums at critical times during the early stages of tumor development or by continuous treatment with antiserums directed to interact with I-J determinants on suppressor cells or suppressor factors. This later mode of therapy also results in a delay in tumor appearance when suboptimal doses of tumor are given. Preferential diminution of suppressor cell precursor activity has also been observed by pretreatment of tumor recipients with low doses of cyclophosphamide. Normal animals so treated are capable of adoptively transferring primarily helper-type activity to tumor-bearing recipients. Decreased tumor growth and prolonged host survival have also been achieved using BCG as a means of augmenting host effector potential. Thus, it is possible to inhibit tumor development in a murine model by modes of immunotherapy which may be relevant to the early treatment of certain human neoplasms.
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