Immune response to inactivated syngeneic mammary adenocarcinoma cells. I. Role and regulation of antibody synthesis in DBA/2 mice.

The immunogenicities of irradiated T1699 murine mammary adenocarcinoma cells (XR-T1699) and mitomycin C-treated T1699 cells (T1699m) were compared with respect to eliciting humoral immunity, cell-mediated immunity, and protection against subsequent sc challenge with untreated T1699 tumor cells (T1699u) in the syngeneic host (DBA/2 mice). Treatment with 10(3)-10(7) T1699m failed to induce any immunity against subsequent challenge with viable T1699u, whereas 10(6)-10(7) XR-T1699 sensitized the host to later challenge with T1699u. Although both T1699m- and XR-T1699-sensitized mice displayed a delayed hypersensitivity response to soluble T1699 antigen as determined by footpad swelling, only XR-T1699-immunized mice developed detectable levels of anti-T1699 antibody, as measured by indirect immunofluorescence. The antibody-dependent cellular cytotoxicity (ADCC) titer of sera from XR-T1699-immunized mice peaked at day 11 and declined by day 20, whereas sera from T1699m- sensitized mice showed no detectable ADCC activity. Sera from mice with progressing T1699u tumors showed high levels of ADCC activity at all times tested. The immunity induced by XR-T1699 injection was shown to be specific for T1699 tumor cells and not limited to the anatomic area of immunization. The results are discussed in terms of the role of antibody as the primary protective mechanism in sensitization in the T1699 tumor model.