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Cellular Immunity to Mammary Tumor Virus in Normal and Tumor-bearing C3H/HeN Mice

Laboratory of Immunodiagnosis, National Cancer Institute, NIH, Bethesda, Maryland 20014

Cellular immunity to mouse mammary tumor virus (MTV) in normal virgin female C3H/HeN-MTV+ (hereafter called C3H+) and C3H/HeN-MTV- (hereafter called C3H-) mice was assessed by the indirect agarose droplet migration inhibition (MI) assay. Spleen cells from C3H+ mice were able to respond to MTV antigens and produced a factor (presumably macrophage MI factor) that inhibited migration of normal mouse peritoneal exudate cells. This reactivity appeared at 14 weeks of age in C3H+ mice but was no longer detectable at 36 weeks. In contrast, reactivity was never displayed by spleen cells of C3H- mice. Injection of 10 µg of MTV in C3H+ or C3H- mice younger than 14 weeks of age induced similar reactivity to MTV antigens in both mouse strains. This pattern of reactivity suggested that normal C3H+ mice are not tolerant to antigens of MTV and that overt infection is required for induction of an immune response. Further investigations were performed to see whether the growth of a syngeneic transplantable mammary tumor (MAT-2) affected the MI response to MTV in both C3H+ and C3H- mice. A response to MTV antigens could be detected in C3H- mice younger than 14 weeks of age, but C3H+ tumor-bearing mice were generally unable to respond to MTV antigens. A similar pattern of results in MI tests with tumor-bearing animals was obtained with a glycoprotein with a molecular weight of 52,000, the major glycoprotein of MTV, as the antigen. The differences in MI reactivity of normal, MTV-immunized, and tumor-bearing C3H+ and C3H- mice that have been observed in these studies indicate that development of cell-mediated immunity to MTV antigens may be dependent on the dose, route, and length of exposure to MTV antigens.

¹ On leave from Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. To whom requests for reprints should be addressed, at Laboratory of Immunodiagnosis, National Cancer Institute, NIH, Building 10, Room 8B07, Bethesda, Md. 20014.

Received 1/18/78. Accepted 4/20/78.