The effect of immunotherapy with extracted tumor antigens on sinecomitant immunity

The fate of hosts after tumor resection depends upon the level of their sinecomitant immunity, which can destroy residual neoplastic cells. In addition, active specific immunotherapy can stimulate the resistance of mice incompletely resected of large tumors and therefore destined to develop recurrent disease. The studies presented herein, assessing host resistance by in vivo tumor challenge and an in vitro growth inhibition assay (GIA) measuring the effect of splenic lymphocytes on 3H-thymidine incorporation into monolayers of sarcoma cells, revealed an antagonistic relationship between sinecomitant immunity and tumor antigen immunotherapy. Treatment of hosts bearing high levels of endogenous sinecomitant immunity with Fraction 15 pI 5.95 partially purified from 3 M KCl extracts by preparative isoelectric focusing, decreased their resistance to tumor challenge and the capacity of their spleen cells to perform in the in vitro GIA. When sinecomitant immunity was not demonstrable, therapy with tumor antigen induced host resistance. If therapy was delayed until sinecomitant immunity had naturally waned, hosts displayed improved resistance toward secondary challenge. These findings suggest that not only does antigen therapy effect tumor resistance by a mechanism independent of sinecomitant immunity, but also these two mechanisms are mutually antagonistic. Therefore, the design of active specific immunotherapy protocols utilizing tumor antigens may depend on the level of the host endogenous sinecomitant resistance.