Yefenof E, Ben-David Y
Leuk Res. 1986;10(7):797-801. doi: 10.1016/0145-2126(86)90300-0.
Adult C57BL/6 (B6) mice exposed to fractionated irradiation or inoculated with a highly leukemogenic RadLV (A-RadLV) develop high incidence of lymphatic leukemias after a latency of 3-5 months. Inoculation of a low leukemogenic RadLV variant (D-RadLV) does not result in lymphoma development unless the animals receive a single, sublethal dose of irradiation. Whereas virus-induced primary lymphomas produce virus, express gp70 and are all immunogenic, those induced by X-rays are devoid of virus expression and are not immunogenic. A-RadLV inoculation into B6 mice is associated with early induction of virus specific, cyclophosphamide sensitive suppressor T cells which are capable of abrogating a potential antitumor immune responsiveness. D-RadLV, on the other hand, induces reactive T lymphocytes that arrest leukemogenesis unless their function is impaired by irradiation. In (B6 X BALB/c)F1 mice both A-RadLV and D-RadLV leukemogenesis depend on sublethal irradiation of the host, and both induce reactive T cells. These results suggest that (a) RadLV and X-ray induced leukemogeneses involve different etiologies. (b) Different leukemogenic treatments evoke different host responses early in latency which can either sustain or interfere with lymphoma progression.
成年C57BL/6（B6）小鼠接受分次照射或接种高致白血病性RadLV（A-RadLV）后，在3至5个月的潜伏期后会出现高发性淋巴白血病。接种低致白血病性RadLV变体（D-RadLV）不会导致淋巴瘤的发生，除非动物接受单次亚致死剂量的照射。虽然病毒诱导的原发性淋巴瘤会产生病毒、表达gp70且具有免疫原性，但X射线诱导的淋巴瘤则缺乏病毒表达且无免疫原性。将A-RadLV接种到B6小鼠体内与早期诱导病毒特异性、对环磷酰胺敏感的抑制性T细胞有关，这些细胞能够消除潜在的抗肿瘤免疫反应。另一方面，D-RadLV诱导反应性T淋巴细胞，这些细胞会阻止白血病的发生，除非它们的功能因照射而受损。在（B6×BALB/c）F1小鼠中，A-RadLV和D-RadLV诱导白血病的发生均依赖于宿主的亚致死照射，且两者都会诱导反应性T细胞。这些结果表明：（a）RadLV和X射线诱导的白血病发生涉及不同的病因。（b）不同的致白血病治疗在潜伏期早期会引发不同的宿主反应，这些反应既可以维持也可以干扰淋巴瘤的进展。
