Uede T, Sato O, Iguchi S, Kikuchi K
No Shinkei Geka. 1981 Mar;9(4):503-8.
The mechanism of the suppression on the cellular immunity was analysed in experimental brain tumor rats. The tumor used in this experiment was a 3-methylcholanthrene induced fibrosarcoma. The tumor cell was inoculated into the caudate nucleus of the rats with a Hamilton microsyringe. When spleen cells from brain tumor rats were added to the PHA blastogenesis system, impairment of the normal lymphoproliferative response to the PHA was detected as early as on the third day and continued until the ninth day after inoculation. After the depletion of glass adherent cells, the residual cells from the spleen could not suppress the normal lymphoblastogenesis by the PHA. After the depletion of T cells by anti-T cell sera and complement, however, the residual cells from the spleen still suppressed the normal lymphoblastogenesis. Glass adherent cells were able to phagocyte the latex particles. From these findings, the suppressor cell responsible for the suppression of the normal lymphoblastogenesis by the PHA was considered to be macrophage and suppressor T cell did not play a role in the suppression of the PHA responses in this experimental model. The sera from brain tumor rats could not inhibit the proliferative responses of lymphocytes to PHA. Thus the possibility of the existence of suppressive factors in the sera was also negligible.
对实验性脑肿瘤大鼠的细胞免疫抑制机制进行了分析。本实验中使用的肿瘤是3-甲基胆蒽诱导的纤维肉瘤。用汉密尔顿微量注射器将肿瘤细胞接种到大鼠的尾状核中。当将脑肿瘤大鼠的脾细胞加入到PHA淋巴细胞转化系统中时，早在接种后第三天就检测到对PHA的正常淋巴细胞增殖反应受损，并持续到第九天。去除玻璃黏附细胞后，脾脏中的残余细胞不能抑制PHA诱导的正常淋巴细胞生成。然而，用抗T细胞血清和补体去除T细胞后，脾脏中的残余细胞仍能抑制正常淋巴细胞生成。玻璃黏附细胞能够吞噬乳胶颗粒。根据这些发现，认为负责抑制PHA诱导的正常淋巴细胞生成的抑制细胞是巨噬细胞，在该实验模型中抑制性T细胞在抑制PHA反应中不起作用。脑肿瘤大鼠的血清不能抑制淋巴细胞对PHA的增殖反应。因此，血清中存在抑制因子的可能性也可忽略不计。
