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Potentiation of Interferon Induction of Class I Major Histocompatibility Complex Antigen Expression by Human Tumor Necrosis Factor in Small Cell Lung Cancer Cell Lines

University of Maryland Cancer Center and Division of Medical Oncology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201

The response of class I major histocompatibility complex antigen expression to in vitro administration of interferon and tumor necrosis factor (TNF-) was measured using class I major histocompatibility complex-deficient small cell lung cancer cell lines. Significant induction also was observed using interferon (IFN-) alone, whereas TNF- alone yielded only modest induction. Classic small cell lung cancer cell lines NCI-H146 and NCI-H209 best demonstrated synergistic HLA and ß₂-microglobulin antigen induction with IFN- and TNF- with the following dose schedule: 3–6 days of TNF- (200 units/ml) followed by 48 h of IFN- (100 IU/ml). Induction was quantitated using an ¹²⁵I-Protein A radioimmunoassay. Synergistic induction of the HLA and ß₂-microglobulin surface antigens on NCI-H146 was also possible with interferon and TNF- but required a higher concentration of the interferon, i.e., 3–6 days of TNF- (200 units/ml) followed by 48 h of interferon (1000 units/ml).

Small cell lung cancer cell line NCI-H146 was further studied for expression of major histocompatibility complex messenger RNA using the optimal doses and sequence of addition of IFN- and TNF- as indicated above. A significant induction with IFN- alone and synergistic induction with both IFN- and TNF- was quantitated for both HLA-A2 and ß₂-microglobulin transcripts using Northern blot analysis. Incubation with relatively low subcytotoxic doses of IFN- and TNF- also resulted in a marked synergistic decrease in c-myc message.

¹ To whom requests for reprints should be addressed, at the University of Maryland Cancer Center, Room 9-045, BRB, 655 W. Baltimore St., Baltimore, MD 21201.

² Supported in part by Grant K08 CA 01067 from the National Cancer Institute, NIH, and a Rizer Memorial Research Grant from the American Cancer Society, Maryland Division.

Received 3/ 9/89. Revised 6/28/89. Accepted 8/16/89.

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