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Comparative Studies on the Induction of Transplantation Resistance in BALB/c and C57BL/6 Mice in Three Murine Leukemia Systems¹

Microbiological Associates, Inc. [J.L.M.], United States Public Health Corps [A.F.], and Drug Evaluation Branch, National Cancer Institute [A.F., J.P.G.], Bethesda, Maryland 20014

Syngeneic X-irradiated Friend, Moloney, and Rauscher (FMR) lymphomas readily induce transplantation resistance in C57BL/6 mice. Similar resistance is more difficult to induce in BALB/c mice. To determine whether this difference in response is due to a lesser immunogenicity of FMR cells of BALB/c origin, C57BL/6 mice were pretreated with viable or X-irradiated BALB/c FMR cells, or with X-irradiated C57BL/6 FMR cells, and were challenged with FMR lymphomas of C57BL/6 origin. The reverse experiments were performed in BALB/c recipients. All FMR lymphomas of both strains induced strong transplantation resistance in C57BL/6 mice. Therefore, FMR lymphomas of BALB/c origin were immunogenic in C57BL/6 mice. However, FMR cells of either strain generally induced only weak or nondetectable resistance in BALB/c mice. X-irradiated FMR lymphomas of both strains released varying amounts of infectious virus when inoculated into BALB/c newborns. Lymphomas releasing lesser amounts of virus were usually the more effective immunogens for the induction of transplantation resistance in BALB/c mice. It was therefore postulated that BALB/c mice were less able than C57BL/6 mice to handle immunologically large quantities of virus. This was substantiated by the markedly greater susceptibility of weanling BALB/c mice than C57BL/6 mice to Rauscher virus, as judged by the induction of splenic enlargement, viremia and death. It is suggested that the inoculation of highly susceptible BALB/c mice with lymphomas that release large quantities of virus may impede or obscure specifically or nonspecifically the immunologic reactivity to a subsequent tumor challenge.

¹ This study was supported by Contract PH-43-64-911 from the Cancer Chemotherapy National Service Center, National Cancer Institute, NIH, USPHS. Presented in part at the 57th Annual Meeting, American Association for Cancer Research, Denver, Colorado, May 26–28, 1966.

Received 2/24/67. Accepted 5/22/67.