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Immunology |
in Rejection of Established Tumors by IL-12
Department of Surgery, University of California, VA Medical Center, San Francisco, California 94121
We have demonstrated previously that established small and large murine MCA207 sarcomas can be completely eradicated by treatment with interleukin (IL) 12 alone and cyclophosphamide plus IL-12 (Cy+IL-12), respectively. The antitumor effect of IL-12/Cy+IL-12 has been found to be dependent on IFN-
and T cells. The role of IFN- in IL-12-induced tumor rejection is unclear, because after IL-12 administration IFN- is produced by multiple cell types, and it acts on most cell types because of the ubiquitous expression of its receptor. Using a T-cell-adoptive transfer model, we show that after IL-12 treatment, tumor-specific T-cell production of IFN- is necessary and sufficient for rejection of established tumors. Furthermore, by testing tumors using IFN--unresponsive tumor cells, we show that tumor cell expression of MHC class I molecules in vivo is abrogated by blocking the response to IFN-. However, tumor response to IFN- is not essential for rejection of established small and large tumors by IL-12 and Cy+IL-12, respectively; neither is it essential for expression of tumor immunogenicity. Our results indicate that the rejection of established tumors by IL-12/Cy+IL-12 is dependent on the induction of a Th1 response producing IFN- that acts on host cells.
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