Clerici E, Bigi G, Garotta G, Porta C, Mocarelli P
J Natl Cancer Inst. 1976 Mar;56(3):513-6. doi: 10.1093/jnci/56.3.513.
Mice bearing Ehrlich ascites tumors and challenged with sheep erythrocytes produced fewer plaque-forming cells than did normal mice. At the same time the immunosuppression developed, the number of T lymphocytes in the thymus and spleen were reduced significantly. In the spleen, the number of B lymphocytes remained constant during carcinogenesis, whereas that of the macrophages increased significantly, as compared to the controls. In this paper, we demonstrated that the mechanism responsible for thymus and spleen depletion of theta antigen-bearing cells had to be ascribed to fewer T-lymphocyte precursors in the bone marrow of mice with cancer. The reduction of T-lymphocyte precursors was probably caused by the same "soluble factor(s)" produced by Ehrlich ascites tumor cells, which also interfered with the proliferation of myelopoietic stem cells in the bone marrow of mice with this neoplasm, as we previously reported. By performing several reconstitution experiments of lethally X-irradiated hosts, we determined that the immunodepression by Ehrlich ascites tumor cells was readily reversible, and the alteration of the T:B lymphocyte ratio in the spleen had a minor function, if any, in the pathogenesis of the immunosuppression.
携带艾氏腹水瘤并受到绵羊红细胞攻击的小鼠产生的空斑形成细胞比正常小鼠少。在免疫抑制发展的同时,胸腺和脾脏中的T淋巴细胞数量显著减少。在脾脏中,B淋巴细胞的数量在致癌过程中保持不变,而与对照组相比,巨噬细胞的数量显著增加。在本文中,我们证明了导致胸腺和脾脏中携带θ抗原细胞耗竭的机制必须归因于患癌小鼠骨髓中T淋巴细胞前体数量的减少。T淋巴细胞前体数量的减少可能是由艾氏腹水瘤细胞产生的相同“可溶性因子”引起的,正如我们之前报道的,这种因子也干扰了患有这种肿瘤的小鼠骨髓中骨髓造血干细胞的增殖。通过对接受致死性X射线照射的宿主进行多次重建实验,我们确定艾氏腹水瘤细胞引起的免疫抑制很容易逆转,并且脾脏中T:B淋巴细胞比例的改变在免疫抑制的发病机制中作用很小(如果有作用的话)。