Apoptosis in rat prostatic adenocarcinoma is associated with rapid infiltration of cytotoxic T-cells and activated macrophages.

Rats transplanted with the androgen-sensitive, syngeneic Dunning R3327 PAP prostatic tumor were castrated and treated with estrogen or vehicle for 4, 12 and 24 hr and for 6 weeks. Tumor growth was retarded by castration and further inhibited by estrogen. Immediately after castration, an increased number of activated macrophages and T-cells were found in parallel with increasing apoptotic tumor cells. Administration of an immunosuppressive drug, FK 506, abolished the growth-inhibitory effects of castration and estrogen. The tumor growth rate correlated negatively with the number of R73- and OX8-positive T-cells and NK cells and with the percentage of ED3-positive macrophages. There was a positive correlation between the percentage of TdT-mediated-dUTP nick end labeling (TUNEL)-positive apoptotic cells and that of ED3-positive cells. Our results suggest that apoptosis of prostatic carcinoma cells induced by endocrine treatment in vivo is partly due to a rapid infiltration by immunocompetent cells.