| Abstract: | Human peripheral blood monocytes possess receptors on their surface for human interferon-gamma (IFN-gamma). Inasmuch as the biologic effects of IFN-gamma are thought to be mediated through binding of the molecule to this receptor, modulation of receptor number may be a means for enhancing the effect of IFN-gamma. We examined this possibility by treating human monocytes in culture with dexamethasone. At a dexamethasone concentration of 200 nM, there was a twofold increase in the number of 125I-recombinant IFN-gamma molecules bound to the cell. An effect was noted at concentrations of dexamethasone greater than 50 nM, and was observed as early as after 18 hr of treatment. The observed effect was the result of both a 50% decrease in receptor number in untreated cells and an increase to pretreatment levels or greater in cells incubated with dexamethasone. These results suggest that dexamethasone may modulate the effects of IFN-gamma on monocytes by changes in receptor number. |
