Varesio L, Herberman R B, Gerson J M, Holden H T
Int J Cancer. 1979 Jul 15;24(1):97-102. doi: 10.1002/ijc.2910240117.
Immune spleen cells from mice injected with murine sarcoma virus (MSV) can produce migration inhibition factor (MIF) in vitro after stimulation with intact tumor cells. We have now found that this effector function can be regulated by suppressor macrophages present in the tumor. The cells from the tumor (CfT) exert a strong suppressive effect even after treatment with anti-Thy 1.2 plus complement but lose this capacity if adherent or phagocytic cells are removed, suggesting that the macrophage is the suppressor cell. The effects of the suppressor cells were exerted on a proliferation-independent function of the lymphocytes, since MIF production, as well as its suppression, occurred even after proliferation of the lymphocytes was blocked by mitomycin-C. The implications of these findings are that macrophages can suppress some early events involved in the activation of lymphocytes by antigen and that they do so through a mechanism that does not relate to the proliferation of the cells.
用鼠肉瘤病毒（MSV）注射的小鼠的免疫脾细胞，在受到完整肿瘤细胞刺激后可在体外产生迁移抑制因子（MIF）。我们现已发现，这种效应功能可受到肿瘤中存在的抑制性巨噬细胞的调节。肿瘤细胞（CfT）即使在用抗Thy 1.2加补体处理后仍具有很强的抑制作用，但如果去除贴壁或吞噬细胞则会失去这种能力，这表明巨噬细胞是抑制性细胞。抑制性细胞的作用作用于淋巴细胞的非增殖依赖性功能，因为即使淋巴细胞的增殖被丝裂霉素-C阻断后，MIF的产生及其抑制仍会发生。这些发现的意义在于，巨噬细胞可以抑制抗原激活淋巴细胞所涉及的一些早期事件，并且它们通过与细胞增殖无关的机制来做到这一点。
