Cooperation of immune lymphoid and reticuloendothelial cells during Listeria monocytogenes-mediated tumor immunity.

Listeria monocytogenes (LM) in admixture with cells from a murine, chemically induced tumor retarded local tumor development in the syngeneic host. Intra-footpad growth of 10(4) tumor cells was equally inhibited by 4 x 10(4) admixed LM in normal or LM-immune mice indicating that concomitant or prior immunity to LM was equally effective in suppressing tumor growth. Development of cellular immunity to viable LM was required for tumor rejection. Mice prevented from developing anti-LM immunity by inoculation of dead bacteria were also incapable of inhibiting tumor growth. Further, a functionally active reticuloendothelial system was essential for nonspecific inhibition of tumor development as temporary "paralysis" of the reticuloendothelial system by a prior injection of 10(9) heat-killed LM reduced the effectiveness of LM-mediated tumor suppression. Histological examination of LM or LM tumor-injected sites revealed a stepwise development of LM-mediated inflammatory reaction of delayed type associated with gradual degeneration of the adjacent tumor cells.