Spontaneous SP1 murine adenocarcinoma cells transfected with the murine 7-interferon (IFN-7) gene expressed IFN-7 (SP1/IFN-7) failed to grow in syngeneic hosts and grew in nude mice. The rejection ot SIM/ IFN-7 cells was related to the amount of IFN-7 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-7. 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 11N>was needed to inhibit tumorigenicity while only 8 units/ml IFN-7 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 sup porting the contention that class I MHC expression is not essential for the rejection response induced by IFN-7. The failure of SP1/IFN-7 cells to protect against a challenge with parent SP1 cells argues that factors other than IFN-7 production or class I MHC expression are needed to induce a protective response against weakly or nonimmunogenic tumor cells.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Feb 1991|
ASJC Scopus subject areas
- Cancer Research