Pozzi L A, Weiser W Y
Department of Medicine, Harvard Medical School, Boston, Massachusetts.
Cell Immunol. 1992 Dec;145(2):372-9. doi: 10.1016/0008-8749(92)90339-q.
A recombinant form of human migration inhibitory factor (rMIF) obtained from COS-1 cells transfected with MIF-specific cDNA is able to activate cultured human peripheral blood monocytes and monocyte-derived macrophages, in a dose-dependent manner to become cytotoxic for tumor cells in vitro. The cytotoxicity exhibited by macrophages treated with rMIF is > or = 30% above that of cells incubated with control supernatants or with media and peaks 72 hr after the addition of tumor targets. rMIF also induces macrophages to produce tumor necrosis factor (TNF-alpha) and interleukin-1 beta (IL-1 beta). These results demonstrate that rMIF is able to modulate macrophage functions and plays a role in cell-mediated immune response.
从用MIF特异性cDNA转染的COS-1细胞中获得的重组人迁移抑制因子（rMIF），能够以剂量依赖的方式激活培养的人外周血单核细胞和单核细胞衍生的巨噬细胞，使其在体外对肿瘤细胞具有细胞毒性。用rMIF处理的巨噬细胞所表现出的细胞毒性比用对照上清液或培养基孵育的细胞高≥30%，并且在添加肿瘤靶标后72小时达到峰值。rMIF还诱导巨噬细胞产生肿瘤坏死因子（TNF-α）和白细胞介素-1β（IL-1β）。这些结果表明，rMIF能够调节巨噬细胞功能，并在细胞介导的免疫反应中发挥作用。
