Yefenof E, Ben-David Y
Cancer Immunol Immunother. 1983;16(1):48-52. doi: 10.1007/BF00199905.
Suppressor cells capable of enhancing tumor growth in vivo and of abrogating a potential anti-tumor immunity in vitro are generated in C57BL/6 mice inoculated with the high-leukemogenic A-RadLV. Mice inoculated with low-leukemogenic D-RadLV do not develop suppressor cells but contain anti-tumor reactive lymphocytes that can inhibit in vivo tumor growth. Cyclophosphamide (CyF) treatment of mice inoculated with A-RadLV hampered suppressor cell function and rendered the animals' lymphocytes responsive to A-RadLV induced tumor cells in vitro. Administration of CyF also reduced leukemia incidence in mice inoculated with A-RadLV, but had no effect on leukemia induction by D-RadLV in irradiated mice. It is suggested that the high leukemogenic activity of A-RadLV depends on the virus' ability to recruit CyF-sensitive suppressor cells early in latency and that tumor progression in mice inoculated with D-RadLV is arrested due to the host immune response.
在接种高致白血病性A-RadLV的C57BL/6小鼠中，会产生能够在体内增强肿瘤生长并在体外消除潜在抗肿瘤免疫的抑制细胞。接种低致白血病性D-RadLV的小鼠不会产生抑制细胞，但含有可抑制体内肿瘤生长的抗肿瘤反应性淋巴细胞。对接种A-RadLV的小鼠进行环磷酰胺（CyF）处理会阻碍抑制细胞功能，并使动物的淋巴细胞在体外对A-RadLV诱导的肿瘤细胞产生反应。给予CyF还降低了接种A-RadLV小鼠的白血病发病率，但对辐照小鼠中D-RadLV诱导的白血病没有影响。有人提出，A-RadLV的高致白血病活性取决于该病毒在潜伏期早期募集对CyF敏感的抑制细胞的能力，并且接种D-RadLV的小鼠中的肿瘤进展因宿主免疫反应而停止。
