Berendt M J, North R J, Kirstein D P
J Exp Med. 1978 Dec 1;148(6):1560-9. doi: 10.1084/jem.148.6.1560.
It was shown that of four syngeneic, murine tumors investigated, only those that evoked the generation of a state of concomitant anti-tumor immunity were susceptible to endotoxin-induced regression. Moreover, the temporal relationship between the generation of concomitant immunity and the onset of susceptibility to endotoxin-induced regression points to the likely possibility that tumor regression depends on the preceding acquisition of the specifically-sensitized, effector T cells that express concomitant immunity. It is suggested that endotoxin-induced hemorrhagic necrosis which invariably precedes tumor regression serves to create conditions inside the tumor that are conducive to the entry and the functioning of effector T cells. It is also suggested that tumor necrosis factor causes hemorrhagic necrosis rather than tumor regression.
结果表明,在所研究的四种同基因小鼠肿瘤中,只有那些能引发伴随抗肿瘤免疫状态的肿瘤对内毒素诱导的消退敏感。此外,伴随免疫的产生与对内毒素诱导消退的易感性开始之间的时间关系表明,肿瘤消退可能取决于先前获得表达伴随免疫的特异性致敏效应T细胞。有人提出,肿瘤消退之前必然发生的内毒素诱导的出血性坏死有助于在肿瘤内部创造有利于效应T细胞进入和发挥作用的条件。也有人提出,肿瘤坏死因子导致出血性坏死而非肿瘤消退。