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From The Salk Institute for Biological Studies, The Armand Hammer Center for Cancer Biology, San Diego, California 92112
Abstract
The nature of the cells effecting in vitro cell-mediated immunity has been examined and compared in a syngeneic and allogeneic tumor system. The tumors used for these different models were the syngeneic W/Fu rat transplantable lymphoma (C58NT)D, induced by Gross virus, and the allogeneic DMBA#8 cell line derived from a chemically-induced F334 rat mammary carcinoma.
In both systems, time course experiments show that cytotoxic effector cells recirculate through the thoracic duct. Maximum cell-mediated cytotoxicity in the lymph occurs at day 7 after immunization, which is close in time to peak cytotoxic activity in the spleen.
Since treatment of spleens immunized with the syngeneic or allogeneic cell line with specific anti-T cell serum markedly decreases cytotoxicity, we conclude that the major effector cell is a thymus-derived lymphocyte.
We did some experiments to decide whether, in addition to T cell killing, there was antibody-dependent cell-mediated cytotoxicity. In the allogeneic system in particular there was some indication that the antibody-directed mechanism may play a role. Following primary (as well as repeated) immunization, a high proportion of allogeneic sera have the capability of inducing specific tumor target lysis by normal spleen cells. In a few instances, similar but weak antibody activity appeared in syngeneic sera only after a booster injection of tumor cells and if harvested after 30 to 50 days. In the syngeneic system it therefore seems likely that only T cells are concerned in the rejection process following primary inoculation of tumor cells, whereas in the allogeneic systems, in addition to cytotoxic T cells, antibody-dependent effector cells also may be involved in tumor cell destruction. This latter conclusion is supported by the finding that anti-T cell serum completely abrogates cytotoxicity in the syngeneic system, while the inhibition is sometimes incomplete in the allogeneic one.
Footnotes
1 Financial support was provided by the National Institutes of Health via research Grant AI 06544 from National Institute of Allergy and Infectious Diseases, and Contract 72-E-3207 from National Cancer Institute. Funds were also provided to The Salk Institute by Dr. Armand Hammer. Gunther Dennert was supported by The American Cancer Society via Grant IM-39, and by The National Cancer Institute via Grant CA 15581-01. Edwin Lennox was partially supported by a grant from The Western Institute for Cancer and Leukemia Research.
2 Present address: ICRF Tumor Immunology Unit, University College London, London, England.
3 To whom reprint requests should be sent.
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