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Cell-mediated Immune Response of Hamsters to Alloantigen and Tumor Antigens of Isologous and Autochthonous Origin during Chemical Carcinogenesis¹

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

The temporal relationship between depression of cell-mediated immunity and papilloma and carcinoma development during treatment with 7,12-dimethylbenz[a]-anthracene (DMBA) was studied. The test antigens used were non-tumor-related allografts and DMBA-pretreated isografts and autografts containing clones of neoplastic cells. Allografts were invariably rejected by DMBA-pretreated recipients, and the allograft survival times increased as a function of tumor burden on animals receiving optimal carcinogen treatment. The survival of carcinogen-pretreated isografts (with early stages of tumor development) was found to depend on immunological competence, as indicated by the prolongation of graft survival on recipients treated with antithymocyte serum. The survival of isografts also increased with the number of DMBA pretreatments and the tumor burden of recipients. The association of tumor burden with depression of the immune response to non-tumor-related and tumor-related antigens is interpreted to be the result of competition between the test antigens and the antigens of developing autochthonous tumors. This interpretation is supported by the findings that DMBA pretreatment of animals did not depress the immune response to autografts containing clones of neoplastic cells. Autograft survival, in contrast to the survival of allografts and isografts, was reduced. The survival was inversely related to the extent of tumor development on autografts prior to grafting. Because of the distinctive host response to autografts it is concluded that the available pool of immunologically uncommitted cells may be the limiting factor in the response against alloantigens and the neoantigens present in isografts. Furthermore, competition for immunologically uncommitted cells may also be functional among autochthonous clones of neoplastic cells of different antigenicities early in DMBA-induced tumor development.

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

Received 8/23/73. Accepted 10/18/73.