Berendt M J, North R J, Kirstein D P
J Exp Med. 1978 Dec 1;148(6):1550-9. doi: 10.1084/jem.148.6.1550.
It was shown that although intravenous administration of bacterial endotoxin caused extensive hemorrhagic necrosis of four different syngeneic murine tumors, only two of these tumors subsequently underwent complete regression: the two that were shown to be immunogeneic as classically defined. An immunologic basis for endotoxin-induced regression was further indicated by the additional findings that regression, but not hemorrhagic necrosis, of the two immunogenic tumors failed to occur in mice that were immunodepressed by whole-body gamma-irradiation, or that were made T-cell deficient by thymectomy and irradiation. That endotoxin-induced regression is T-cell mediated was suggested by the findings that tumor regression was followed by a state of long-lived immunity to a tumor cell challenge implant, and with the possession by the host of T cells that were capable of passively transferring this state of immunity to normal recipients. It is concluded that although parenteral injection of endotoxin causes hemorrhagic necrosis of most solid murine tumors, it is only those tumors that are immunogenic enough to evoke the generation of T-cell-mediated immunity which subsequently go on to completely regress.
研究表明，尽管静脉注射细菌内毒素会导致四种不同的同基因小鼠肿瘤出现广泛的出血性坏死，但其中只有两种肿瘤随后完全消退：这两种肿瘤被证明是经典定义的免疫原性肿瘤。全身γ射线照射致免疫抑制的小鼠，或胸腺切除并照射致T细胞缺陷的小鼠，两种免疫原性肿瘤会发生出血性坏死，但不会消退，这一额外发现进一步表明内毒素诱导消退存在免疫学基础。肿瘤消退后对肿瘤细胞攻击植入产生长期免疫状态，且宿主拥有能够将这种免疫状态被动转移给正常受体的T细胞，这些发现提示内毒素诱导的消退是由T细胞介导的。结论是，尽管胃肠外注射内毒素会导致大多数实体小鼠肿瘤发生出血性坏死，但只有那些免疫原性足以引发T细胞介导免疫产生的肿瘤随后才会完全消退。
