Regulation of the steady state level of FcγRI mRNA by IFN-γ and dexamethasone in human monocytes, neutrophils, and U-937 cells

L. Pan, D. B. Mendel, J. Zurlo, P. M. Guyre

Research output: Contribution to journalArticle

Abstract

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 languageEnglish (US)
Pages (from-to)267-275
Number of pages9
JournalJournal of Immunology
Volume145
Issue number1
StatePublished - Jan 1 1990

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Regulation of the steady state level of FcγRI mRNA by IFN-γ and dexamethasone in human monocytes, neutrophils, and U-937 cells'. Together they form a unique fingerprint.

  • Cite this