Association of rheumatoid factor production with FcγRIIIa polymorphism in Taiwanese rheumatoid arthritis

Abstract

Summary Fcγ receptors (FcγR) impact upon the development of inflammatory arthritis through immune complex stimulation and proinflammatory cytokine production. FcγRIIa, FcγRΙΙΙa and FcRγIIIb polymorphisms were genotyped in 212 rheumatoid arthritis (RA) patients and 371 healthy control subjects using an allelic-specific polymerase chain reaction (PCR). No significant skewing in the distribution of FcγRIIa H/R131, FcγRIIIa F/V158 and FcγRIIIb NA1/NA2 was found between RA patients and healthy control subjects. However, a significant skewing distribution of the FcγRIIIa F/V158 polymorphism was observed between rheumatoid factor (RF)-positive versus RF-negative RA patients (P = 0·01). The low-affinity FcγRIIIa F158 allele seems to have a protective role in RF production, in comparison with the FcγRIIIa V158 allele (P = 0·004; OR = 0·485; 95% CI: 0·293–0·803). A high frequency of FcγRIIIa F/F158 was identified in RA patients with negative RF compared with RF-positive patients (for FF158 versus FV158 + VV158; P = 0·002; OR = 0·372; 95% CI: 0·194–0·713). In addition, no association was found between FcγRIIa H/R131, FcγΡIIIa F/V158 and FcγRIIIb NA1/NA2 polymorphisms and other clinical parameters. The results of this study suggest that three activating FcγRs polymorphisms lack association with RA but FcγIIIa F/V158 polymorphism may influence RF production and IgG RF immune complex handling in Taiwanese RA patients.