Belardelli F, Gresser I, Maury C, Maunoury M T
Int J Cancer. 1982 Dec 15;30(6):821-5. doi: 10.1002/ijc.2910300622.
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 interferon-treated 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.
我们试图确定在接受干扰素治疗的小鼠腹腔中，何种宿主机制导致Friend白血病细胞（FLC）数量迅速减少。通过注射放射性标记的FLC，我们发现，与对照小鼠相比，接受干扰素治疗的个体小鼠体内放射性损失更大。因此，由于细胞破坏，从接受干扰素治疗的小鼠腹腔中回收的细胞可能更少。仅在肿瘤细胞接种前的时期用干扰素治疗小鼠，可赋予一定程度的抗肿瘤活性，尽管该方案远不如在肿瘤细胞接种后每天开始并持续使用干扰素治疗有效。我们无法将含有来自接受干扰素治疗的供体小鼠的巨噬细胞和淋巴细胞的腹腔灌洗液中的任何抗肿瘤活性转移给接种肿瘤的受体小鼠。腹腔内接种二氧化硅颗粒会破坏巨噬细胞功能并可能影响NK细胞活性，但并未消除干扰素的抗肿瘤活性。我们认为，干扰素通过并非由易于回收的可溶性因子或细胞毒性细胞介导的机制诱导宿主介导的抗肿瘤作用。这种由干扰素强力诱导的宿主机制的本质仍然未知。
