The therapeutic significance of concomitant antitumor immunity

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Abstract
It is shown that progressive growth of the SA1 sarcoma in its semisyngeneic AB6F1 host results in the generation of concomitant immunity to growth of a tumor challenge implant, and in the generation of T cells in the spleen capable, on passive transfer, of causing regression of an established tumor in γ-irradiated recipients, but not in normal recipients. T cells that passively transferred concomitant immunity against an established tumor were first generated around day 6 of tumor growth, reached peak numbers on day 9, and slowly decreased in number thereafter. They were of the Ly-1−2+ phenotype, in that they were functionally eliminated by treatment with monoclonal anti-Ly-2 antibody and complement, but not by treatment with anti-Ly-1 antibody and complement. The paradoxical ability of T cells from a donor with a relatively large tumor to cause the regression of a tumor in sublethally γ-irradiated recipeints is explained with reference to the facts that the recipient tumor was only half as large as the donor tumor at the time of passive transfer, and that the recipient was incapable of generating suppressor T cells that would function to inhibit the expression of adoptive immunity.

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