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Temporal down‐regulation of FcγRIII expression and Fcγ receptor‐mediated phagocytosis in human monocyte‐derived macrophages induced by TNF‐α and IL‐1β

Effects of tumor necrosis factor (TNF‐α) and interleukin‐1β (IL‐1β) on the expression of Fcγ receptors (FcγRs) and on FcγR‐mediated phagocytosis in human monocyte‐derived macrophages (MDMs) have been determined. Treatment of MDMs with TNF‐a (400 pg/ml) or IL‐1β (400 pg/ml) for 80 min decreased cell surface FcγRIII expression, as measured by flow cytometry (FAGS), while the levels of surface FcγRI and FcγRII remained unchanged. Surface FcγRIII expression remained depressed for 7 h after exposure of MDMs to either cytokine but then rose progressively until, by 24 h of stimulation, the levels were at least as high as those on unstimulated cells. In parallel with cell surface FcγRII I levels, phagocytosis of immunoglobulin G‐opsonized fluorescent beads, as measured by FAGS, decreased and then increased over time after stimulation of MDMs with TNF‐α while the opsonin‐independent phagocytic activity was unchanged, suggesting that among the three classes of Fcγ receptors on macrophages, FcγRIII may play a critical role in regulating opsonic phagocytosis. After treatment with IL‐1β, both opsonic and nonopsonic phagocytic activities of MDMs were significantly decreased, regardless of FcγRIII levels. FAGS analysis of rhodamine‐phalloidin‐stained MDMs showed that after incubation with IL‐1β, but not TNF‐α, the content of Factin declined in MDMs, coinciding with inhibition of particle phagocytosis. Rapid down‐regulation and subsequent recovery of macrophage FcγRIII expression following cytokine stimulation could serve as a novel regulatory mechanism employed by inflammatory cells in host defensc. J. Leukoc. Biol. 55: 702–710; 1994.