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Reduced Tumorigenicity of Murine Tumor Cells Secreting -Interferon Is Due to Nonspecific Host Responses and Is Unrelated to Class I Major Histocompatibility Complex Expression¹

Departments of Cell Biology [N. E., B. H., T. I.] and Medical Oncology [P. F.], University of Texas M. D. Anderson Cancer Canter, Houston, Texas 77030

Spontaneous SP1 murine adenocarcinoma cells transfected with the murine -interferon (IFN-) gene expressed IFN- (SP1/IFN-) failed to grow in syngeneic hosts and grew in nude mice. The rejection of SP1/IFN- cells was related to the amount of IFN- 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-K^k negative but express class I antigens when producing IFN-. 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- was needed to inhibit tumorigenicity while only 8 units/ml IFN- 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-. The failure of SP1/IFN- cells to protect against a challenge with parent SP1 cells argues that factors other than IFN- production or class I MHC expression are needed to induce a protective response against weakly or nonimmunogenic tumor cells.

¹ Supported in part by USPHS Grants 41525 and 39853 and by a grant from Sid Richardson Foundation.

² To whom requests for reprints should be addressed, at University of Texas M. D. Anderson Cancer Center, Department of Cell Biology, 1515 Holcombe Blvd., Box 173, Houston, TX 77030.

Received 9/20/90. Accepted 12/ 6/90.

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