Development of teratocarcinoma does not impair immunization of mice against Listeria monocytogenes. Endotoxin injection a short time before tumor cell inoculation allows the growth of teratocarcinoma in non syngenic mice despite immune stimulation. In contrast with this absence of impaired systematic immunity, teratocarcinoma cells were found to repulse macrophages in vitro. This effect on macrophages was also found with three other malignant cells and with trophoblast cells. In vivo, teratocarcinoma cells were found to impair local inflammation. These cells and other malignant cells are able to produce a compound(s) of molecular weight between 103 and 104, which prevents inflammatory reaction. These results suggest that mouse teratocarcinomas and other tumors by-pass the host immunological system of surveillance by at least two mechanisms: a direct toxic effect on macrophages and the release of an inhibitor of inflammation. The possible relations between these properties of malignant cells and physiological functions of trophoblast are discussed.Like many tumors, mouse teratocarcinomas can be transplanted and grown in syngenic adult mice (1), although they possess a surface antigen considered "foreign" by these animals (2). In this paper, we report the results of experiments designed to analyze the mechanism allowing teratocarcinoma cells to by-pass the host immunological system of surveillance. This mechanism appears to operate at least at two levels, i.e., diapedesis and macrophage-tumor cell interaction. The role of cellular immunity in host resistance against tumor is well established (6). In order to determine whether or not the growth of teratocarcinoma results in a systemic decrease in cellular immunity, we have followed the capacity of mice, harboring such tumors, to be immunized against Listeria monocytogenes. This immunity is known to depend on the activation of macrophages by sensitized T lymphocytes (thymus-derived lymphocytes) (7). The results of such an experiment are reported in Table 1