IFN‐α1 gene transfection completely abolishes the tumorigenicity of murine B16 melanoma cells in allogeneic DBA/2 mice and decreases their tumorigenicity in syngeneic C57BL/6 mice

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Abstract
The murine B16 melanoma (H-2b) was transfected with a retroviral vector containing the mouse IFN-α1 gene. IFN-α1-transfected cells produced IFN-α in vitro and exhibited an altered phenotype characterized by a decreased rate of multiplication, enhanced expression of H-2 antigens, an antiviral state to VSV, and decreased pigmentation. Control and IFN-α1-transfected cells were tested for their ability to grow in syngeneic (H-2b) CS7B1/6 and allogeneic (H-2d) DBA/2 mice. IFN-α1producing B16 clones were less tumorigenic after s.c, i.p., and i.v. routes of injection than IFN-non-producer BI6 clones in syngeneic CS7B1/6 mice. IFN-α1-producing B16 cells were, however, totally rejected by allogeneic DBA/2 mice regardless of the routes and inocula tested, while control B16 cells grew in and killed DBA/2 mice. The total rejection of IFN-α1-transfected B16 cells in allogeneic mice appeared to be dependent on T cells as these cells grew in DBA/2 nude mice. Incubation of IFN-α-producing clones with anti-mouse IFN-α/β prior to injection into C57BI/6 mice did not enhance their tumorigenicity. Likewise, injection of C57BI/6 and DBA/2 mice with antibody to IFN-α/β did not enhance the tumorigenicity of IFN-α1-transfected cells. C57B1/6 mice immunized with irradiated IFN-α1 cells were only slightly protected against a subsequent challenge with parental B16 cells. In contrast, DBA/2 mice immunized with irradiated IFN-α1 cells exhibited tumor-specific, long-lasting immunity to subsequent challenge with parental B16 cells.

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