IFN-β1b augments glucocorticoid-induced suppression of tumor necrosis factor-α production by increasing the number of glucocorticoid receptors on a human monocytic cell line

We studied the effect of recombinant interferon-β1b (IFN-β1b) 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-β1b augments the suppressive effect that dexamethasone has on the stimulated production of tumor necrosis factor-α (TNF-α), most likely related to the increased number of GCR observed after exposure to IFN-β1b. This provides a possible clue to the mechanism of action of IFN-β in multiple sclerosis.

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