Youdim S
Cancer Res. 1977 Feb;37(2):572-7.
Listeria monocytogenes (LM) in admixture with B-16 melanoma suppresses local tumor development in syngeneic C57BL/6 mice. In vitro, LM-immune peritoneal and splenic cells are cytotoxic to B-16. Induction of cell-mediated immunity to LM antigens are required for the killing effect, since effector cells from LM-"immune" athymic nude mice are unable to kill tumor cells in vitro. Further, elimination of macrophages by a specific antiserum plus complement abrogates the cytotoxic effect of peritoneal cells. Peritoneal or splenic adherent or nonadherent cells are not cytotoxic, whereas combination of these two cell populations in the presence of the specific antigen can kill the B-16 target cells. A factor, probably lymphotoxin, released by the intact effector cells in the culture fluid mediates tumor cell destruction in vitro. Production of this factor requires cooperation of macrophages with specifically sensitized thymus-derived cells.
单核细胞增生李斯特菌（LM）与B - 16黑色素瘤混合后，可抑制同基因C57BL/6小鼠体内局部肿瘤的发展。在体外，对LM免疫的腹膜细胞和脾细胞对B - 16具有细胞毒性。由于来自LM“免疫”无胸腺裸鼠的效应细胞在体外无法杀死肿瘤细胞，因此对LM抗原的细胞介导免疫诱导是产生杀伤作用所必需的。此外，用特异性抗血清加补体清除巨噬细胞可消除腹膜细胞的细胞毒性作用。腹膜或脾的贴壁细胞或非贴壁细胞均无细胞毒性，而这两种细胞群体在特异性抗原存在的情况下联合可杀死B - 16靶细胞。培养液中完整效应细胞释放的一种因子（可能是淋巴毒素）在体外介导肿瘤细胞的破坏。该因子的产生需要巨噬细胞与特异性致敏的胸腺来源细胞的协同作用。
