Bowlin T L, Rosenberger A L, McKown B J, Davis G F, Sunkara P S
Int J Immunopharmacol. 1986;8(2):131-6. doi: 10.1016/0192-0561(86)90052-4.
The objective of the present investigation was to evaluate the effect of DFMO (DL-alpha-difluoromethylornithine HCl H2O) administration on tumoricidal effector cell generation by IFN or IFN inducers in vivo. DFMO administration reduces both splenic leukocyte and peritoneal macrophage polyamine levels. In tumor bearing (B16 melanoma) mice, DFMO administration did not impair splenic natural killer (NK) cell augmentation, assessed against NK sensitive YAC-1 target cells, by IFN alpha/beta or the IFN inducers tilorone and polyriboinosinic: polyribocytidilic acid (poly I:C). Tumoricidal macrophage activation by IFN alpha/beta was similarly uninhibited by DFMO. However, only tumoricidal macrophage not NK cell activity was observed which could kill the B16 melanoma target cells. These results indicate that DFMO is not immunosuppressive regarding antitumor cytolytic cell induction in vivo.
本研究的目的是评估给予二氟甲基鸟氨酸盐酸盐一水合物（DFMO）对体内干扰素（IFN）或IFN诱导剂产生杀肿瘤效应细胞的影响。给予DFMO可降低脾脏白细胞和腹腔巨噬细胞中的多胺水平。在荷瘤（B16黑色素瘤）小鼠中，通过IFNα/β或IFN诱导剂泰洛龙和聚肌苷酸:聚胞苷酸（poly I:C）评估，给予DFMO不会损害针对NK敏感的YAC-1靶细胞的脾脏自然杀伤（NK）细胞增殖。IFNα/β对杀肿瘤巨噬细胞的激活同样不受DFMO抑制。然而，仅观察到可杀死B16黑色素瘤靶细胞的杀肿瘤巨噬细胞活性，而非NK细胞活性。这些结果表明，在体内抗肿瘤溶细胞性细胞诱导方面，DFMO不具有免疫抑制作用。
