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Autogenous Immunity to Endogenous RNA Tumor Virus Antigens in Mice with a Low Natural Incidence of Lymphoma¹

Carcinogenesis Program, Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830

The immune reactivity to endogenous (wild-type) RNA tumor virus-related antigen(s) was evaluated in RF mice, a strain with a low natural incidence of lymphoma. The purposes were to determine whether maintained humoral immunity could be detected and to evaluate the response with respect to the immune-mediated pathogenesis of glomerulosclerosis and incidence of tumors of lymphatic origin. Measurements of detectable murine leukemia virus antigen in the thymus and spleen were correlated with the development of immune competence, glomerulosclerosis, and the incidence of lymphoid neoplasia. Also, the specificity of the antibody that lodged in the kidney was determined by elution and indirect immunofluorescence with Gross virus-infected cells. A marked decrease in detectable murine leukemia virus antigen in thymus and spleen was found to correlate with development of immunological competence of the spleen as assayed by de novo germinal-center formation, antigen localization, and immune elimination from serum, which in turn correlated with occurrence of glomerulosclerosis. The antibody in the kidney was determined to be specific for Gross virus antigen(s). The role of this autogenous immunity may be considered to be beneficial in the RF mouse, as data correlating natural lymphoid neoplasia with severity of immune-complex glomerulosclerosis indicates that an inverse relationship is established in aged animals.

¹ Research supported jointly by the National Cancer Institute and the United States Atomic Energy Commission under contract with Union Carbide Corporation.

Received 4/21/72. Accepted 6/28/72.

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