BCG Immunopotentiation of an Antitumor Response: Evidence for a Cell-Mediated Mechanism 2

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Abstract
BCG-immunopotentiated antitumor immunity was studied in a model in which irradiated murine tumor cells, mastocytoma P815, were injected into subcutaneous sites prepared by a prior injection of BCG; challenge in a distant footpad was used as an indicator of specific resistance. The onset of antitumor immunity correlated with the proliferation of lymph node cells draining the immunization sites and the development of delayed type hypersensitivity (DTH) to the tumor. Tuberculin hypersensitivity, however, was depressed during the evolution of DTH to the tumor. Antitumor immunity was transferred locally with spleen or lymph node cells that were sensitive to anti-θ sera and complement but not to antiIg and complement. They had velocity sedimentation rates in a bovine serum albumin gradient of 3.9–5.9 mm/hour and were relatively resistant to vinblastine at the peak of the immune response. Sera from immunized mice failed to confer antitumor immunity either in vitro or on transfer in vivo.

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