Induction of major histocompatibility class I antigens by interferons in undifferentiated F9 cells

• Published in: Journal of cellular physiology Vol. 130; no. 2; p. 276
• Main Authors: Wan, Y J, Orrison, B M, Lieberman, R, Lazarovici, P, Ozato, K
• Format: Journal Article
• Language: English
• Published: United States 01.02.1987
• Subjects: Animals; Cell Differentiation; Cell Line; Genes; HLA Antigens - biosynthesis; HLA Antigens - genetics; Interferon Type I - pharmacology; Interferon-gamma - pharmacology; Major Histocompatibility Complex; Mice; Nucleic Acid Hybridization; Receptor, Epidermal Growth Factor - metabolism; RNA, Messenger - genetics; Teratoma
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041300214

Mouse embryonal carcinoma F9 cells, upon treatment with interferons (IFNs), express major histocompatibility (MHC) Class I antigens, which are otherwise not expressed in these cells. Both IFN-gamma and IFN-alpha/beta increase the steady-state level of Class I mRNA within 60 min of the treatment which leads to the subsequent surface expression of the H-2Kb and H-2Db antigens, suggesting that undifferentiated F9 cells express IFN receptors. IFNs induce Class I antigen expression in F9 cells in a highly selective manner: unlike retinoic acid treatment which also stimulates the antigen expression, IFNs induce neither morphological differentiation, increased binding of epidermal growth factor, nor reduction of expression of stage specific embryonic antigen. The effect of IFNs is reversible; removal of IFNs, even after prolonged exposures, results in a rapid loss of the Class I gene expression. Further, Class I mRNA induction is not inhibited by cycloheximide, suggesting possible independence from de novo protein synthesis. This Class I antigen induction in F9 cells is reminiscent of that observed in somite stage mouse embryos by IFN treatment and may offer a model system to study activation of MHC genes during development.