The high affinity IgG FcR FcγRI, CD64, plays important roles in the immune response. FcγRI is predominantly expressed on monocytes and macrophages, and barely detectable on neutrophils. rIFN-γ markedly increases the expression of FcγRI on neutrophils, monocytes, macrophages and myeloid cell lines such as U-937, HL-60, and THP-1. Glucocorticoids inhibit the augmentation of FcγRI expression by rIFN-γ on neutrophils and myeloid cell lines, but enhance the augmentation of FcγRI expression by rIFN-γ on monocytes. In this study, we examined the effect of rIFN-γ and dexamethasone (Dex) on the steady state level of FcγRI mRNA in U-937 cells, neutrophils, and monocytes by hybridizing total RNA with the FcγRI cDNA probe, p135. We found that the amount of FcγRI mRNA increased within 1 h of treatment with rIFN-γ in all three cell types. This initial induction of FcγRI mRNA by rIFN-γ was completely blocked by an inhibitor of RNA synthesis, actinomycin D, suggesting that the rIFN-γ-mediated induction of FcγRI mRNA is dependent on gene transcription. Dex, used in combination with rIFN-γ, partially blocked the induction of FcγRI mRNA by rIFN-γ in U-937 cells and neutrophils, but caused a synergistic increase in FcγRI mRNA levels in monocytes. The inhibitory effect of Dex on the steady state level of FcγRI mRNA in U-937 cells was blocked by an inhibitor of protein synthesis, cycloheximide, suggesting that Dex-induced proteins were involved in the regulation of FcγRI expression. This study indicates that the regulation of FcγRI expression on U-937 cells, neutrophils, and monocytes by rIFN-γ and Dex occurs, at least in part, at the mRNA level. rIFN-γ increases the steady state level of FcγRI mRNA through a common pathway among U-937 cells, neutrophils, and monocytes, whereas the effect of Dex on rIFN-γ-induced FcγRI mRNA is cell-type specific.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1990|
ASJC Scopus subject areas
- Immunology and Allergy