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Objectives. Levels of immunoglobulin G (IgG) Fc receptors (FcγRs) affect the activity and function of monocytes/macrophages when binding IgG-containing immune complexes. Hence, the expression level of FcγRs on monocytic cells may influence inflammation in patients with rheumatoid arthritis (RA). In this study the expression levels of FcγRI, IIa and IIIa on peripheral blood monocytes of RA patients were compared with those of healthy controls and related to patient and disease characteristics and the use of disease-modifying anti-rheumatic drugs (DMARDs). In addition, FcγR expression levels were determined on RA synovial fluid macrophages and compared with those in RA peripheral blood.
Methods. Mononuclear cells from peripheral blood and synovial fluid were isolated and FcγR expression levels on CD14-positive cells were analysed by flow cytometry. The effects of patient and disease characteristics and the use of DMARDs were assessed.
Results. A high expression level of FcγRIIa and high percentages of FcγRIIIa-expressing monocytes were found in RA patients with a high erythrocyte sedimentation rate. DMARD-naive early RA patients had higher FcγRIIa expression levels but a similar amount of FcγRIIIa-positive monocytes compared with RA patients using DMARDs. In synovial fluid, FcγRIIa expression levels were lower than in RA peripheral blood, whereas the percentage of FcγRIIIa-positive monocytic cells was higher in synovial fluid than in peripheral blood.
Conclusions. These data point to the involvement of FcγRs, specifically FcγRIIa and IIIa, in the immune response of RA and suggest that FcγR expression levels are susceptible to modulation by DMARD therapy.

Objective. To investigate whether apocynin, 1-(4-hydroxy-3-methoxyphenyl)ethanone, is able to diminish inflammation-induced cartilage destruction in rheumatoid arthritis (RA), studied in a human in vitro model.
Methods. Apocynin was added to cultures of RA peripheral blood mononuclear cells (PBMNC). Cartilage-destructive activity was determined by addition of culture supernatant to tissue samples of human articular cartilage. In addition, the proliferation of PBMNC, their production of tumour necrosis factor alpha (TN-Fα), interleukin (IL)-1 and IL-10, and T-cell production of interferon gamma (IFN-γ) and IL-4, as measures for T1 and T2 cell activity, were determined.
Results. Apocynin was able to counteract RA PBMNC-induced inhibition of cartilage matrix proteoglycan synthesis, while no effect on inflammation-enhanced proteoglycan release was found. The effect was accompanied by a decrease in IL-1 and TNF-α production by the MNC. No effect on T-cell proliferation was found, but the production of IFN-γ, IL-4 and T-cell-derived IL-10 was strongly diminished. Most important, apocynin did not show any direct adverse effects on chondrocyte metabolism; on the contrary, it diminished the release of proteoglycans from the cartilage matrix.
Conclusion. Apocynin in vitro inhibits inflammation-mediated cartilage destruction without having adverse effects on cartilage. The latter may be an advantage of apocynin over many other non-steroidal anti-inflammatory drugs. Therefore, apocynin might have an added beneficial effect in protecting RA patients from joint destruction.

Rozema: Celgene: Other: Financial support for visiting MDS Foundation conference.

Bergh: Sanofi: Membership on an entity's Board of Directors or advisory committees, Other: speakers fee; Eli Lilly: Membership on an entity's Board of Directors or advisory committees, Other: speakers fee; Amgen: Membership on an entity's Board of Directors or advisory committees, Other: speakers fee; UCB: Membership on an entity's Board of Directors or advisory committees, Other: speakers fee.

No relevant conflicts of interest to declare.