Article Text


THU0170 Immunoglobulin g fc-receptor (fcgr) iiia polymorphisms and disease expression in rheumatoid arthritis
  1. JG Brun1,
  2. TM Madland1,
  3. CA Vedeler2
  1. 1Department of Rheumatology
  2. 2Department of Neurology, Haukeland University Hospital, Bergen, Norway


Background Fc receptors for IgG (FcγR) modulate immune responses. Fcγ receptors are expressed on various leukocytes and contain allelic polymorphisms with different capacity for IgG binding and phagocytosis. The FcγR polymorphisms have been implicated as genetic factors that may influence the susceptibility to autoimmune disease. FcγRIII has two isoforms (A and B) and is encoded by genes on chromosome 1. For FcγRIIIA, the presence of the valine (V) allele confers a higher receptor affinity for IgG1, IgG3 and IgG4 than does the presence of the phenylalanine (F) allele.

Objectives We investigated the distribution of the FcγRIIIA alleles in rheumatoid arthritis (RA), and whether they were related to disease expression and severity.

Methods Ninety-six controls and 114 patients fulfilling ACR criteria for RA were genotyped for FcγRIIIA polymorphisms using PCR. Physician’s global assessment of RA type estimated RA disease expression. In addition, usual measures of disease activity were recorded.

Results Crosstabulation of the FcγRIIIA genotypes V/V and V/F combined vs the F/F genotype showed that more patients with aggressive RA than expected had the V/V and V/F genotypes (P < 0.05). The FcγRIIIA V/F genotype and the V allele was slightly more frequent among RA patients than among controls. This finding however, was not statistically significant. We found no significant associations with the clinical and laboratory variables of disease activity.

Conclusion The results of previous studies regarding FcγRIIIA in RA are not consistent. The present findings of a more severe disease among patients homo- and heterozygous for the valine (V) allele, and the suggested tendency of more than expected V/V and V/F genotypes among RA patients as compared to controls, lend support to the notion of FcγRIIIA as a possible disease susceptibility and disease-modifying gene in RA.

Statistics from

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.