Tunru I S, Suzuki H, Yano S
First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Int J Cancer. 1991 Jun 19;48(4):568-73. doi: 10.1002/ijc.2910480415.
The enhancing effect of macrophages on interleukin-2 (IL-2)- and IL-4-induced murine lymphokine-activated killer (LAK) activity was investigated in this study. Peritoneal macrophages significantly enhanced LAK activity generated from accessory cell-depleted splenic lymphocytes in both IL-2 and IL-4 cultures. This effect was dependent on the number of macrophages and was not replaced by a factor derived from macrophages or lymphocytes. Macrophages enhanced IL-2- and IL-4-induced LAK activity against both natural killer (NK)-sensitive (YAC-I, P388D1) and NK-resistant (P815) tumor cells. Negative selection of cells with antibodies and complement showed no differences in surface markers between IL-2 LAK effectors and IL-4 LAK effectors generated in the presence of macrophages. These results suggest that the same LAK effector subsets can be enhanced by macrophages in either IL-2 or IL-4 cultures.
本研究探讨了巨噬细胞对白细胞介素-2(IL-2)和IL-4诱导的小鼠淋巴因子激活的杀伤细胞(LAK)活性的增强作用。在IL-2和IL-4培养物中,腹腔巨噬细胞显著增强了从辅助细胞耗竭的脾淋巴细胞产生的LAK活性。这种作用取决于巨噬细胞的数量,且不能被源自巨噬细胞或淋巴细胞的因子所替代。巨噬细胞增强了IL-2和IL-4诱导的针对天然杀伤(NK)敏感(YAC-I、P388D1)和NK抗性(P815)肿瘤细胞的LAK活性。用抗体和补体对细胞进行阴性选择显示,在巨噬细胞存在的情况下产生的IL-2 LAK效应细胞和IL-4 LAK效应细胞之间的表面标志物没有差异。这些结果表明,相同的LAK效应细胞亚群在IL-2或IL-4培养物中均可被巨噬细胞增强。