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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

Uitdehaag, B.M.; Hoekstra, K.; Koper, J.W.; Polman, C.H.; Dijkstra, C.D.

Journal of Interferon and Cytokine Research the Official Journal of the International Society for Interferon and Cytokine Research 21(3): 133-135

2001

ISSN/ISBN: 1079-9907
PMID: 11331035
DOI: 10.1089/107999001750133113
Accession: 010776737
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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.

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