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.
ASJC Scopus subject areas
- Cancer Research