Spontaneous SP1 murine adenocarcinoma cells transfected with the murine γ-interferon (IFN-γ) gene expressed IFN-γ (SP1/IFN-γ) failed to grow in syngeneic hosts and grew in nude mice. The rejection of SP1/IFN-γ cells was related to the amount of IFN-γ produced and appeared to be mediated primarily by nonspecific cellular mechanisms, although some role for T-cells in the afferent arm of this response is possible. SP1 cells are H2-Kk negative but express class I antigens when producing IFN-γ. However, class I major histocompatibility complex (MHC) expression, while likely necessary, was insufficient in itself to prevent tumor growth since secretion of >64 units/ml IFN-γ was needed to inhibit tumorigenicity while only 8 units/ml IFN-γ could induce class I antigens. Similar results were obtained with the murine colon carcinoma CT-26, a tumor that constitutively expresses class I MHC antigens, further supporting the contention that class I MHC expression is not essential for the rejection response induced by IFN-γ. The failure of SP1/IFN-γ cells to protect against a challenge with parent SP1 cells argues that factors other than IFN-γ production or class I MHC expression are needed to induce a protective response against weakly or nonimmunogenic tumor cells.

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Supported in part by USPHS Grants 41525 and 39853 and by a grant from Sid Richardson Foundation.

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