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JOHAN G. BRUN, TOR M. MADLAND, and CHRISTIAN A. VEDELER

ABSTRACT.

Objective. Fc receptors for IgG (FcgR) modulate immune responses. FcgR are expressed on various leukocytes and contain allelic polymorphisms with different capacity for IgG binding and phagocytosis. We investigated the distribution of FcgRIIA, FcgRIIIA, and FcgRIIIB polymorphisms in rheumatoid arthritis (RA) and whether they were related to disease expression and severity.

Methods. Ninety-six controls and 114 patients fulfilling American College of Rheumatology (ACR) criteria for RA were genotyped for FcgRIIA, IIIA, and IIIB using polymerase chain reaction. Physician's global assessment of RA type estimated RA disease expression. In addition, usual measures of disease activity were recorded.

Results. The genotype and allele frequencies did not differ significantly between the RA patients and the controls. Patients homo or heterozygous for the FcgRIIA arginine (R) allele had significantly more aggressive RA and swollen joints than patients homozygous for the FcgRIIA histidine (H) allele. Although there was a tendency of more severe disease among patients homo or heterozygous for the FcgRIIIA valine allele, there were no significant findings with the disease activity for the FcgRIIIA and FcgRIIIB genotypes.

Conclusion. FcgRIIA is implicated as a possible disease modifying gene in RA. Individuals homozygous for the FcgRIIA R allele have less efficient binding of IgG2 subclasses than individuals homozygous for the H allele. Less effective processing of circulating immune complexes in RA patients homozygous for the FcgRIIA R allele may therefore contribute to a more unfavorable course. (J Rheumatol 2002;29:1135-40)

Key Indexing Terms:

RHEUMATOID ARTHRITIS
FC-RECEPTORS
DISEASE SEVERITY
GENETICS

From the Department of Rheumatology and Department of Neurology, Haukeland University Hospital, Bergen, Norway.

J.G. Brun, MD, PhD, Associate Professor; T.M. Madland, MD, Senior Rheumatologist; C.A. Vedeler, MD, PhD, Professor, Department of Neurology.

Address reprint requests to Dr. J.G. Brun, Department of Rheumatology, Haukeland University Hospital, N-5021 Bergen, Norway. E-mail: jgbr@haukeland.no

Submitted March 19, 2001; revision accepted December 28, 2001.