Glucocorticoid hormones inhibit DNA synthesis and enhance interferon production in human lymphoid cell line

• Published in: Nature (London) Vol. 282; no. 5740; p. 736
• Main Authors: Adolf, G R, Swetly, P
• Format: Journal Article
• Language: English
• Published: England 13.12.1979
• Subjects: Burkitt Lymphoma - immunology; Cell Division - drug effects; Cell Line; Dexamethasone - pharmacology; DNA - biosynthesis; Dose-Response Relationship, Drug; Glucocorticoids - pharmacology; Humans; Hydrocortisone - pharmacology; Interferons - biosynthesis; Prednisolone - pharmacology; Time Factors; Triamcinolone - pharmacology
• ISSN: 0028-0836
• DOI: 10.1038/282736a0

Although buffy coat leukocytes have been the prime source of human interferon, cells of the Burkitt lymphoma line Namalwa are increasingly used for the large scale production of interferon. On induction with Sendai virus or Newcastle disease virus, Namalwa cells produce a substantial quantity of interferon which contains predominantly the leukocyte antigenic species and minor amounts of fibroblast-type interferon. We have recently demonstrated that inducers of erythropoietic differentiation in Friend cells are able to enhance interferon synthesis in Namalwa cells when added to cultures larger than or equal to 24 h before interferon induction by Sendai virus. The most potent compounds, n-butyrate, stimulated interferon production about 30-fold and has also been independelty described by others. All active compounds inhibited DNA synthesis in Namalwa cells and the extent of inhibition apparently paralleled the stimulatory potency of the respective compound. Induction of differentiation of Friend cells can be antagonised by various steroid hormones, which by themselves have no measurable effects on these cells. In contrast, we report here that glucocorticoid hormones inhibit DNA synthesis in Namalwa cells and augment Sendai virus-induced interferon synthesis.