Landolfo S, Herberman R B, Holden H T
J Immunol. 1977 Apr;118(4):1244-8.
Spleen cells from C57BL/6 mice immunized with murine sarcoma virus (MSV) are capable of producing migration inhibition factor (MIF) in response to stimulation with a specific tumor-associated antigen prepared by solubilization with 3 M KCL. We have previously demonstrated that this response is T cell-dependent. Further investigations into the effector cells involved in the production of MIF have revealed that spleen cells from mice immunized with MSV cannot produce MIF when stimulated with tumor extract if the population has been previously depleted of macrophages. However, the response can be restored by adding nonimmune syngeneic macrophages but not by allogeneic macrophages. The inability of allogeneic macrophages to provide this function was not due to their increased suppressor activity since in mixing experiments they did not interfere with the ability of immune spleen cells to produce MIF. Furthermore, they were not defective since they could supply this "cooperative function" to appropriate F1 mice. The results indicate that macrophages are required for stimulation of MIF by soluble tumor antigens and that for efficient interaction the macrophages and lymphocytes must share some genetic similarities.
用鼠肉瘤病毒（MSV）免疫的C57BL/6小鼠的脾细胞，在受到用3M KCl溶解制备的特定肿瘤相关抗原刺激时，能够产生迁移抑制因子（MIF）。我们之前已经证明这种反应是T细胞依赖性的。对参与MIF产生的效应细胞的进一步研究表明，如果先前已耗尽巨噬细胞群体，那么用MSV免疫的小鼠的脾细胞在用肿瘤提取物刺激时不能产生MIF。然而，通过添加同基因非免疫巨噬细胞可以恢复这种反应，而异基因巨噬细胞则不能。异基因巨噬细胞无法提供这种功能并非由于其抑制活性增加，因为在混合实验中它们并不干扰免疫脾细胞产生MIF的能力。此外，它们并无缺陷，因为它们可以为合适的F1小鼠提供这种“协同功能”。结果表明，可溶性肿瘤抗原刺激产生MIF需要巨噬细胞，并且为了实现有效相互作用，巨噬细胞和淋巴细胞必须具有一些遗传相似性。
