Thiel K, Genovesi E V, Iglehart J D, Bolognesi D P, Weinhold K J
Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710.
Adv Exp Med Biol. 1988;239:169-83. doi: 10.1007/978-1-4757-5421-6_17.
Infection by an attenuated replication-competent murine retrovirus (Friend leukemia virus-FLV4), but not other non-transforming retroviruses, stimulated rejection of transplantable thymomas (RL-cell line) and subsequent tumor immunity in syngeneic mouse recipients. FLV-infected RL-cells (RL-FLV) were unaltered in their in vitro growth, and grew progressively to kill sublethally irradiated animals and nude mice. Primary RL-FLV rejection was due to induction of increased natural killer (NK)-cell activity limited to peritoneal sites of tumor inoculation with a minor cytolytic macrophage population. Syngeneic mutant beige (NK-deficient) mice similarly rejected RL-FLV cells with increased peritoneal NK-cell activity and acquired immunity to the parental RL-tumor. While RL-FLV stimulated far greater peritoneal NK activity than did other tested retrovirus-infected RL-cells, the inherent susceptibility of these cells to lysis by normal NK cells was not altered by virus. RL-FLV induced NK effectors showed an indiscriminate lysis pattern that was independent of target cell type and retrovirus expression.
感染一种具有复制能力的减毒鼠逆转录病毒（Friend白血病病毒-FLV4），而非其他非转化逆转录病毒，可刺激同基因小鼠受体排斥可移植性胸腺瘤（RL细胞系）并随后产生肿瘤免疫。感染FLV的RL细胞（RL-FLV）在体外生长未发生改变，并逐渐生长以杀死亚致死剂量照射的动物和裸鼠。原发性RL-FLV排斥反应是由于诱导自然杀伤（NK）细胞活性增加，这种增加仅限于肿瘤接种的腹膜部位，同时伴有少量溶细胞性巨噬细胞群体。同基因米色突变（NK缺陷）小鼠同样通过增加腹膜NK细胞活性排斥RL-FLV细胞，并获得对亲代RL肿瘤的免疫力。虽然RL-FLV比其他测试的逆转录病毒感染的RL细胞刺激了更强的腹膜NK活性，但这些细胞被正常NK细胞裂解的固有敏感性并未因病毒而改变。RL-FLV诱导的NK效应细胞表现出一种无差别裂解模式，该模式独立于靶细胞类型和逆转录病毒表达。
