Neutrophils from the synovial fluid of patients with rheumatoid arthritis express the high affinity immunoglobulin G receptor, FcγRI (CD64): role of immune complexes and cytokines in induction of receptor expression

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Abstract
Neutrophils isolated from the synovial fluid of 16/24 patients with rheumatoid arthritis expressed FcγRI (CD64), the high-affinity receptor for monomeric immunoglobulin G (IgG), on their cell surface. Receptor expression ranged from 17% to 168% of the level of expression obtained after incubation of control blood neutrophils with 100 U/ml interferon-γ (IFN-γ) for 24 hr in vitro. Similarly, mRNA for FcγRI was detected in synovial fluid neutrophils from 12/15 patients and transcript levels ranged from 5% to 200% of the values obtained after treatment of blood neutrophils with IFN-γ for 4 hr in vitro. No surface expression nor mRNA were detected in freshly isolated blood neutrophils from either patients or from healthy controls. Addition of cell-free synovial fluid to control blood neutrophils induced both mRNA and surface expression of FcγRI to levels that were comparable to those achieved after addition of IFN-γ. Neither soluble nor insoluble immune complexes appeared to be involved in induction of FcγRI expression in spite of the ability of these complexes to induce protein biosynthesis. Synovial fluid-induced expression of FcγRI was partially blocked by incubation with neutralizing IFN-γ antibodies, whilst neutralizing interleukin (IL)-6 antibodies had little effect. Levels of IFN-γ measured within these synovial fluids ranged from 0 to 2·7 U/ml, well within the range known to induce neutrophil FcγRI expression. These data thus indicate that gene expression in synovial fluid neutrophils is selectively activated as the cells enter the diseased joint. Furthermore, these data indicate that induced expression of FcγRI may alter the ability of infiltrating neutrophils to respond to IgG-containing immune complexes present in these joints.