IFN-beta1b augments glucocorticoid-induced suppression of tumor necrosis factor-alpha production by increasing the number of glucocorticoid receptors on a human monocytic cell line.
We studied the effect of recombinant interferon-beta1b (IFN-beta1b) on the sensitivity to glucocorticoids (GC) and on the number of GC receptors (GCR) in the human monocytic cell line THP-1. We found that IFN-beta1b augments the suppressive effect that dexamethasone has on the stimulated production of tumor necrosis factor-alpha (TNF-alpha), most likely related to the increased number of GCR observed after exposure to IFN-beta1b. This provides a possible clue to the mechanism of action of IFN-beta in multiple sclerosis.
Uitdehaag
B M
BM
Department of Neurology, Free University, Amsterdam, The Netherlands. bmj.uitdehaag@azvu.nl
Hoekstra
K
K
Koper
J W
JW
Polman
C H
CH
Dijkstra
C D
CD
D001665:Binding Sites; D002460:Cell Line; D003907:Dexamethasone / Q000819:agonists / Q000378:metabolism / Q000494:pharmacology; D005938:Glucocorticoids / Q000819:agonists* / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D000068556:Interferon beta-1a; D000068576:Interferon beta-1b; D016899:Interferon-beta / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D009103:Multiple Sclerosis / Q000378:metabolism; D011485:Protein Binding; D011965:Receptors, Glucocorticoid / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D005938:Glucocorticoids; D008070:Lipopolysaccharides; D011965:Receptors, Glucocorticoid; D014409:Tumor Necrosis Factor-alpha; D000068576:Interferon beta-1b; D016899:Interferon-beta; D003907:Dexamethasone; D000068556:Interferon beta-1a