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Acquired Immunological Tolerance and Carcinogenesis by the Mammary Tumor Virus. II. Immune Responses Influencing Growth of Spontaneous Mammary Adenocarcinomas<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref>

1969; Oxford University Press; Linguagem: Inglês

10.1093/jnci/42.2.321

1460-2105

Donald L. Morton, Leon Goldman, David A. Wood,

Virus-based gene therapy research

Adult hybrid (C3H × C57BL)F1 mice neonatally infectcd with the mammary tumor virus (MTV) are much more susceptible to the growth of transplanted mammary adenocarcinomas than MTV-free hybrids. Immune factors influencing the growth of mammary carcinomas were investigated in an attempt to relate the enhanced tumor growth in MTV+ mice and the resistance of MTV− mice to immunological events. Immunosuppression by total-body irradiation abolished the resistance against tumor growth in MTV− mice, but had little or no effect on tumor growth in MTV+ mice. The ability of lymphoid cells from MTV− mice to transfer resistance against tumor growth to MTV+ mice was tested in neutralization and adoptive immunity experiments. Neutralization experiments revealed that spleen cells from immune MTV− mice rejecting a mammary tumor transplant or spleen cells from normal MTV− mice could completely or partially inhibit tumor growth in MTV+ mice. However, spleen cells from MTV+ mice did not inhibit tumor growth. Inoculation of MTV-infected extracts of C3H lactating mammary tissue, as previously found to induce tolerance in newborn mice, elicited immunity against transplanted mammary adenocarcinomas in adult MTV− mice. These data are consistent with the hypothesis that all spontaneous mammary adenocarcinomas contain a common MTV-related tumor antigen which is antigenic in MTV− mice, but neonatal infection with the MTV induces acquired immunological tolerance to this antigen in MTV+ mice. The immunogenicity of this common tumor antigen in MTV− mice and the acquired immune tolerance to this antigen in MTV+ mice best explain the resistance and susceptibility of these mice to the growth of transplanted spontaneous mammary adenocarcinomas.