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and B Cell Dependent1
* Cancer Research Section, Department of Experimental Pathology, University of Bologna, Bologna, Italy;
Istituti Ortopedici Rizzoli, Bologna, Italy;
Aging Research Center, G. D’Annunzio University Foundation, Chieti, Italy; and
Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy
A vaccine combining IL-12 and allogeneic mammary carcinoma cells expressing p185neu completely prevents tumor onset in HER-2/neu transgenic BALB/c mice (NeuT mice). The immune protection elicited was independent from CTL activity. We now formally prove that tumor prevention is mainly based on the production of anti-p185neu Abs. In the present studies, NeuT mice were crossed with knockout mice lacking IFN-
production (IFN-–/–) or with B cell-deficient mice (µMT). Vaccination did not protect NeuT-IFN-–/– mice, thus confirming a central role of IFN-. The block of Ab production in NeuT-µMT mice was incomplete. About one third of NeuT-µMT mice failed to produce Abs and displayed a rapid tumor onset. By contrast, those NeuT-µMT mice that responded to the vaccine with a robust production of anti-p185neu Ab displayed a markedly delayed tumor onset. In these NeuT-µMT mice, the vaccine induced a lower level of IgG2a and IgG3 and a higher level of IgG2b than in NeuT mice. Moreover, NeuT-µMT mice failed to produce anti-MHC class I Abs in response to allogeneic H-2q molecules present in the cell vaccine. These findings show that inhibition of HER-2/neu carcinogenesis depends on cytokines and specific Abs, and that a highly effective vaccine can rescue Ab production even in B cell-deficient mice.
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