Youdim S, Sharman M
J Immunol. 1976 Nov;117(5 Pt.2):1860-5.
Spleen (SC) and peritoneal cells (PC) from C57BL/6 mice immune to Listeria monocytogenes (LM) have a marked cytotoxic effect on the in vitro growth of B-16 melanoma. Cytotoxicity to B-16 is mediated by the interacting semsitized thymus-derived (T) lymphocytes and macrophages (Mchi) or adherent cells. Separation of immune SC or PC into their adherent and nonadherent components, depletion of the adnerent cells or elimination of the theata-bearing cells from an enriched T cell population all result in the abrogation of cytotoxicity, whereas, recombination of T cells and Mchi re-establishes this effect. Three modes of Mchi/T cell interactions occur: 1) LM immune peritoneal or splenic T cells interact or synergize with their respective adherent cells to become cytotoxic to B-16; 2) combination of peritoneal Mchi and splenic T cells are noncollaborative and therefore noncytotoxic; 3) the cooperative effect of spleen T cells with Mchi are suppressed or inhibited by addition of peritoneal Mchi. Splenic Mchi, however, are neither uncooperative nor inhibitory when interacting with peritoneal T cells. Normal adherent cells can substitute for immune cells in all the cell-cell interactions with similar end results. These results demonstrate that specifically sensitized T cells interact with Mchi for expression of LM-induced nonspecific tumor cell destruction in vitro, however, such interactions may also be noncooperative or suppressive, thus resulting in tumor cell proliferation.
对单核细胞增生李斯特菌(LM)免疫的C57BL/6小鼠的脾脏(SC)细胞和腹腔细胞(PC)对B-16黑色素瘤的体外生长具有显著的细胞毒性作用。对B-16的细胞毒性由相互作用的致敏胸腺来源(T)淋巴细胞和巨噬细胞(Mchi)或黏附细胞介导。将免疫的SC或PC分离为黏附成分和非黏附成分,去除黏附细胞或从富集的T细胞群体中消除携带θ的细胞,均会导致细胞毒性消失,而T细胞和Mchi的重组则可重新建立这种效应。Mchi/T细胞相互作用有三种模式:1)LM免疫的腹腔或脾脏T细胞与其各自的黏附细胞相互作用或协同作用,从而对B-16产生细胞毒性;2)腹腔Mchi和脾脏T细胞的组合不协同,因此无细胞毒性;3)脾脏T细胞与Mchi的协同效应会因添加腹腔Mchi而受到抑制。然而,脾脏Mchi与腹腔T细胞相互作用时既不产生不协同作用也不产生抑制作用。在所有细胞间相互作用中,正常黏附细胞可替代免疫细胞,且产生相似的最终结果。这些结果表明,特异性致敏的T细胞与Mchi相互作用,以表达体外LM诱导的非特异性肿瘤细胞破坏,然而,这种相互作用也可能不协同或具有抑制作用,从而导致肿瘤细胞增殖。