Serum from Fischer rats immunized with 107 cytolytic spleen cells from syngeneic rats bearing the 13762A mammary adenocarcinoma inhibits specific cell-mediated cytotoxicity (CMC). The blocking activity is first detected 5 to 7 days after immunization; peak activity is reached 5 days later. Immunization with spleen cells depleted of T lymphocytes by heterologous anti-T lymphocyte serum and complement abrogates the blocking response. The blocking factor specifically inhibits lysis of the mammary tumor; it does not inhibit lysis of a Maloney sarcoma virus-induced tumor cells (MSVT) or allogeneic fibroblasts by specifically immune spleen cells. Sephacryl S-200 chromatography and immunoadsorption to rabbit anti-rat IgG or anti-rat µ-chain columns indicate that 10 days after immunization, 30% of the blocking activity is IgM and 70% is IgG.

The IgG-blocking activities from animals bearing the 13762A tumor and from animals immunized with lymphocytes from tumor-bearing animals have identical inhibitory specificities. Ascites tumor inocula contained up to 14% host lymphocytes. Depletion of T lymphocytes from the inocula abrogate the early appearance of IgG-blocking activities and prolong animal survival. We interpret these results to suggest that the IgG-BF in sera from 13762A mammary tumor-bearing rats is induced by a small number of immune T cells contaminating the ascites tumor inoculum. It is considered likely, but remains unproven, that anti-receptor antibody-like blocking factors also occur in spontaneously arising tumors.

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