Klein G
Natl Cancer Inst Monogr. 1976 Nov;44:109-13.
There is excellent evidence for the belief that immune surveillance mechanisms prevent the outgrowth of potentially neoplastic cells induced by horizontally transmitted, ubiquitous, potentially oncogenic viruses, indigenous to natural populations. Polyoma virus in mice, Marek's disease in the chicken, Herpesvirus saimiri in the squirrel monkey, and the Epstein-Barr virus in man are examples. There is much less evidence for immune surveillance against chemically induced tumors. It is argued that surveillance against the virus-induced tumors may have evolved by the selective fixation of appropriate immune responsiveness (IR) genes. It is important to distinguish between the breakdown of an existing surveillance mechanism, e.g., by immunosuppresion, and the lack of immune recognition, due to the deficiency of the IR gene equipment. Presently available in vitro lymphocytotoxicity tests are not yet developed to the point where they can reliably distinguish between these alternatives.
有充分的证据支持这样一种观点，即免疫监视机制可防止由水平传播的、普遍存在的、天然种群中固有的潜在致癌病毒诱导的潜在肿瘤细胞生长。小鼠中的多瘤病毒、鸡中的马立克氏病病毒、松鼠猴中的猴疱疹病毒以及人类中的爱泼斯坦-巴尔病毒都是例证。针对化学诱导肿瘤的免疫监视证据则少得多。有人认为，针对病毒诱导肿瘤的监视可能是通过适当免疫反应（IR）基因的选择性固定而进化而来的。区分现有监视机制的崩溃（例如通过免疫抑制）和由于IR基因装备不足导致的免疫识别缺失很重要。目前可用的体外淋巴细胞毒性试验尚未发展到能够可靠区分这些情况的程度。
