Wirth J J, Levy M H, Wheelock E F
J Immunol. 1976 Dec;117(6):2124-30.
Silica, an agent predominantly toxic for macrophages, inoculated i.v. to Friend leukemia virus (FLV)-infected mice, blocks the FLV-leukemosuppressive effects of chlorite-oxidized oxyamylose (COAM)-statolon treatment. FLV-infected, COAM-statolon-treated mice that have received silica and have failed to suppress FLV leukemia produced normal amounts of interferon, but did not make antibodies cytotoxic for FLV leukemic cells. Transfer of untreated spleen cells, splenic T cells, or thymocytes from mice with suppressed FLV erythroleukemia to FLV-infected mice treated with silica and COAM-statolon restores the humoral immune response to FLV antigens and results in leukemosuppression. Thus, T lymphocytes from mice with suppressed erythroleukemia participate in FLV leukemosuppression either directly as effector cells, or indirectly as helper cell in the production of antibodies to FLV antigens.
二氧化硅是一种主要对巨噬细胞有毒的物质，经静脉注射到感染了弗瑞德白血病病毒（FLV）的小鼠体内，会阻断亚氯酸盐氧化淀粉（COAM）-司他洛酮治疗对FLV白血病的抑制作用。接受了二氧化硅且未能抑制FLV白血病的FLV感染、COAM-司他洛酮治疗的小鼠产生正常量的干扰素，但未产生对FLV白血病细胞具有细胞毒性的抗体。将未处理的脾细胞、脾T细胞或胸腺细胞从FLV红白血病得到抑制的小鼠转移到经二氧化硅和COAM-司他洛酮治疗的FLV感染小鼠体内，可恢复对FLV抗原的体液免疫反应并导致白血病抑制。因此，来自红白血病得到抑制的小鼠的T淋巴细胞要么直接作为效应细胞参与FLV白血病抑制，要么间接作为辅助细胞参与产生针对FLV抗原的抗体。
