Bursuker I, North R J
J Exp Med. 1984 May 1;159(5):1312-21. doi: 10.1084/jem.159.5.1312.
This study shows that surgical removal of the meth A fibrosarcoma from its semisyngeneic host fails to result in postexcision immunity to growth of a tumor implant unless the host already has acquired a mechanism of concomitant immunity to growth of an implant. Therefore, tumor excision does not cause immunity to be generated but preserves a mechanism of concomitant immunity that already exists and which otherwise would eventually undergo down-regulation under the influence of suppressor T cells. Removal of the tumor after it has grown large enough to cause the T cell-mediated suppression of concomitant immunity does not result in the reemergence of immunity. Instead, the host remains unable to generate concomitant immunity to a second tumor for a long period of time and retains, for at least 31 d, suppressor T cells able to passively transfer suppression to appropriate recipients. Like the suppressor T cells responsible for active suppression of concomitant immunity, the suppressor T cells responsible for "memory" suppression are of the Ly-1+2- phenotype. The results indicate that progressive tumor growth results in a state of immunological tolerance of tumor-specific, transplantation antigens that can persist in the apparent absence of tumor antigens.
本研究表明,从半同基因宿主中手术切除甲基胆蒽诱导的纤维肉瘤,除非宿主已获得对植入肿瘤生长的伴随免疫机制,否则切除术后不会产生对肿瘤植入生长的免疫。因此,肿瘤切除不会导致免疫产生,而是保留了一种已存在的伴随免疫机制,否则该机制最终会在抑制性T细胞的影响下发生下调。在肿瘤生长到足以引起T细胞介导的伴随免疫抑制后将其切除,不会导致免疫再次出现。相反,宿主在很长一段时间内仍无法对第二个肿瘤产生伴随免疫,并至少在31天内保留能够将抑制作用被动转移给合适受体的抑制性T细胞。与负责主动抑制伴随免疫的抑制性T细胞一样,负责“记忆”抑制的抑制性T细胞具有Ly-1+2-表型。结果表明,肿瘤的进行性生长导致肿瘤特异性移植抗原的免疫耐受状态,这种状态在明显没有肿瘤抗原的情况下仍可持续存在。