Background/Purpose: We have previously demonstrated that Fc gamma receptor(FcgR) IIIb(CD16b) polymorphisms were associated with infusion reaction in rheumatoid arthritis(RA) patients. While CD16b is mainly expressed on the surface of neutrophils, mast cells, role of FcgRs on monocytes in RA patients has not been fully elucidated. We hypothesized that FcgRs might play important roles in the interaction between immune complexes and monocytes. Aim of this study is to elucidate role of FcgRs expressed on monocytes and determine their clinical significance in RA patients.

Methods: Heparinized venous blood was obtained from 48 RA patients and 12 healthy controls(HC). Surface expression of CD16(FcgR III), CD16b, CD32(FcgRII) and CD64(FcgRI) molecules on CD14+ cells were measured by flow cytometry. FcgR IIIb are recognized by anti-CD16b antibody(3G8), but for detection of FcgR IIIa, anti-CD16 antibody(1D3) which can react with both FcgR IIIa and IIIb were used. Percentage of positive cells and mean fluorescence intensity(MFI) for each FcgRs were calculated. They were analyzed on association with clinical parameters, such as erythrocyte sedimentation rate(ESR), serum anti-cyclic citrullinated peptide antibody(ACPA) titer.

Results: Both percentages of CD16+ and CD16b+ cells on CD14+ monocytes were significantly increased in RA patients(18.7±8.0% and 8.5±6.5%) compared with HC(13.3±4.9% and 4.4±3.0%)(p=0.025 and p=0.027). These results suggest that CD16 is upregulated, completely different from CD32 on monocytes in RA. Moreover, CD64 MFI on CD14+ monocytes from RA patients(39.0±9.4) was significantly higher than that of HC(30.8±7.1)(p=0.011). Interestingly, CD64 MFI and percentage of CD16+ cells strongly correlated with ESR(p=0.0016 and p=0.035). CD64 expression itself also correlated with ACPA(p=0.044). On the other hand, CD64 MFI correlated with CD16-expressing cells(p=0.049), but didn’t correlated with CD16b(p=0.24).

Conclusion: We found CD16 and CD64 were aberrantly upregulated on CD14+ monocytes in RA patients. Clinically, CD16b upregulation together with its functional polymorphism may participate in adverse reaction such as infusion reaction, and CD64 and CD16a rather may relate to inflammation and autoantibody production in RA.