Jimenez J J, McCall C A, Cirocco R E, Yunis A A
Department of Medicine, University of Miami School of Medicine, Florida, FL 33101.
J Biol Response Mod. 1990 Jun;9(3):300-4.
We have previously demonstrated that the successful transfer of rat chloroleukemia (Mia C51) cells to newborn rats is related to the host's inability to generate adequate levels of differentiation factor (DF). Thus, when the appropriate amount of DF was injected into rats bearing MIA C51 cells, the development of chloroleukemia was aborted. In the present study, we provide evidence that stimulation of endogenous differentiation activity (DA) production by the administration of a biologic response modifier (Imuvert) will like-wise abort the development of chloroleukemia. Imuvert at 50 micrograms/ml had no direct effect on growth, viability, or differentiation of MIA C51 cells. However, when monocytes from young rats or adult rats were stimulated with Imuvert in vivo or in vitro, there was significant increase in DA production. Treatment of young rats with Imuvert aborted the development of chloroleukemia from transplanted MIA C51 cells. It is concluded that stimulation of endogenous DA production may provide a potentially useful approach in the treatment of leukemia.
我们之前已经证明，将大鼠氯白血病（Mia C51）细胞成功移植到新生大鼠体内与宿主无法产生足够水平的分化因子（DF）有关。因此，当向携带MIA C51细胞的大鼠注射适量的DF时，氯白血病的发展就会停止。在本研究中，我们提供证据表明，通过给予生物反应调节剂（免疫康）刺激内源性分化活性（DA）的产生同样会阻止氯白血病的发展。50微克/毫升的免疫康对MIA C51细胞的生长、活力或分化没有直接影响。然而，当用免疫康在体内或体外刺激幼鼠或成年大鼠的单核细胞时，DA的产生会显著增加。用免疫康治疗幼鼠可阻止移植的MIA C51细胞引发氯白血病的发展。结论是，刺激内源性DA的产生可能为白血病的治疗提供一种潜在有用的方法。
