Host immunity to mycoplasma antigens introduced into B16 melanoma cells: Effect on tumor growth rate and metastasis

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Abstract
Immunization of syngeneic C57BL/6 mice with X-irradiated Bl6 melanoma cells was previously shown to elicit antibodies specific to viral antigens on the melanoma cells. When immunized mice were challenged with viable subcutaneous transplants of B16 melanoma cells that formed non-metastatic tumors in normal mice, tumors failed to develop in some mice, but there was a high incidence of lung metastasis in mice with progressively growing tumors. To determine whether protective immunity and/or enhanced metastasis were the consequences of immune responses specific for inherent tumor-associated viral antigens, non-metastatic B16 melanoma cells were deliberately infected withMycoplasma arginini. The result was incorporation of perpetuating antigens that elicited, in mycoplasma-immunized mice, humoral and cell-mediated immune responses to infected (B16-M+) but not uninfected (B16-M−) cells. When mycoplasma-immunized mice were challenged with B16-M+ and B-16M− subcutaneous transplants, only B16-M+ tumors were rendered slower-growing and appreciably more metastatic. By contrast, in mice immunized against uninfected B16 melanoma cells, both B16-M+ and B16-M− tumors grew more slowly, and metastasized to a greater extent, than corresponding tumors in unimmunized mice. Enhanced metastasis was not experimentally separable from reduced tumor growth rate and was not simply the consequence of a longer period of tumor growth. Evidence suggests that host immunity does not directly promote metastasis, but that reduced tumor growth rates resulting from protective immunity are more conducive to successful dissemination of metastases.