Antitumor effects of interferon in mice injected with interferon‐sensitive and interferon‐resistant friend leukemia cells. II. Role of host mechanisms
Antitumor effects of interferon in mice injected with interferon‐sensitive and interferon‐resistant friend leukemia cells. II. Role of host mechanisms
复制标题
注射干扰素敏感型和干扰素耐药型白血病细胞的小鼠体内干扰素的抗肿瘤作用。
DOI：
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发表时间：
1982
影响因子：
6.4
通讯作者：
M. Maunoury
中科院分区：
文献类型：
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作者：
F. Belardelli;I. Gresser;C. Maury;M. Maunoury
我们试图确定哪些宿主机制负责诱导干扰素治疗小鼠腹腔中Friend白血病细胞（FLC）数量的快速减少。通过注射放射性标记的FLC，我们发现个体干扰素治疗小鼠的放射性损失大于对照小鼠。因此，由于细胞破坏，很可能从干扰素治疗小鼠的腹腔中回收的细胞较少。仅在肿瘤细胞接种前用干扰素治疗小鼠可产生一定程度的抗肿瘤活性，尽管该方案的有效性远低于在肿瘤细胞接种后开始干扰素治疗并每天继续治疗的情况。我们无法将含有巨噬细胞和淋巴细胞的腹腔冲洗液从干扰素处理的供体小鼠转移到肿瘤接种的受体小鼠。二氧化硅颗粒的腹膜内接种，它破坏巨噬细胞的功能，并可能影响NK细胞的活性，但不能消除干扰素的抗肿瘤活性。我们认为，干扰素诱导宿主介导的抗肿瘤作用的机制，而不是由容易恢复的可溶性因子或细胞毒性细胞介导的。这种有效的干扰素诱导宿主机制的性质仍然未知。
We have attempted to determine what host mechanisms are responsible for inducing a rapid decrease in the number of Friend leukemia cells (FLC) in the peritoneal cavity of interferon‐treated mice. By injecting radiolabelled FLC, we showed that there was a greater loss of radioactivity from individual interferon‐treated mice than from control mice. Thus, it was likely that fewer cells were recovered from the peritoneal cavity of interferontreated mice because of cell destruction. Treatment of mice with interferon limited to the period preceding tumor‐cell inoculation conferred some degree of antitumor activity, although this regimen was far less effective than when interferon treatment was initiated and continued daily after tumor‐cell inoculation. We have been unable to transfer any antitumor activity with peritoneal washings containing macrophages and lymphocytes from interferon‐treated donor mice to tumor‐inoculated recipient mice. Inoculation of silica particles i.p., which destroys macrophage function and may affect NK cell activity, did not abrogate interferon's antitumor activity. We suggest that interferon induces a host‐mediated antitumor effect by mechanisms which are not mediated by easily recoverable soluble factors or by cytotoxic cells. The nature of this potent interferon‐induced host mechanism remains unknown.