The possibility that C’3 participates in tumor rejection was investigated in DBA/2 mice previously immunized against L1210 leukemia and in Swiss mice previously immunized against Ehrlich’s adenocarcinoma. In both the cases, animals treated with an appropriate dose of cobra venom factor to produce a C’3 depletion for some days after the tumor challenge, developed the neoplasia and had a mortality rate analogous to that of non-immunized animals. Studies on the peritoneal washing cells obtained at different times after the challenge revealed that in C’3 depleted immunized mice IgM are present on lymphocytes, macrophages and tumor cells, as in the immunized controls, but no contact between the cells and no macrophage phagocytosis were observed and the number of tumor cells increased progressively. These findings indicate that C’3 is critically involved in the rejection of the experimental tumors considered.
The relationship between untreated, irradiated and heat-killed Ehrlich ascites cells and peritoneal macrophages was studied. At different time intervals, peritoneal washing fluids were observed with a dark field-equipped microscope and were used to prepare Leighton tubes. Histological preparations were made from mesenteric lymph nodes. While heat-killed cancer cells were immediately phagocytized by peritoneal macrophages, the phagocytosis of irradiated cancer cells started only after about 72 h. Pyroninophylic lymphoblasts in mesenteric lymph nodes appeared earlier in animals inoculated with heat-killed ascites cells. No phagocytosis by peritoneal macrophages and no histological modification in lymph nodes were observed in animals injected with untreated cancer cells. Mechanisms by which living homologous cancer cells can avoid phagocytosis by macrophages are discussed.
Some aspects of the immunogenicity of the Lewis lung (3LL) carcinoma in C57BL/6 mice are reported. Immediately after i.m. tumor transplant, and for approximately 24 h, tumor antigens were found in the blood stream. They were observed again on the 5th-6th day, when circulating tumor cells could also be noticed. Soluble immune complexes were detected in the blood sera of tumor-bearing mice from the 11th day, indicating that the host had reacted to the neoplastic antigen stimulation with immunoglobulin synthesis. Furthermore, tumor antigens were observed on some circulating lymphocytes, as well as in the thymus and in the spleen. In spleen sections, atypical mitoses also showed the presence of tumor cells. We obtained the in vitro binding of 3LL-antigens, present in 3 M KCl-solubilized extracts, to normal T lymphocytes prepared from healthy C57BL/6 mice. The possibility that circulating T lymphocytes aspecifically bind tumor antigens, carrying them to the thymus, is discussed.
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