Rheumatology 2003; 42: 681-688
© 2003 British Society for Rheumatology
Report |
Fc
receptor expression levels on monocytes are elevated in rheumatoid arthritis patients with high erythrocyte sedimentation rate who do not use anti-rheumatic drugs
1 Rheumatology and Clinical Immunology and
2 Department of Immunology/Immunotherapy Laboratory, University Medical Center Utrecht, Utrecht, The Netherlands
Objectives. Levels of immunoglobulin G (IgG) Fc receptors (Fc
Rs) affect the activity and function of monocytes/macrophages when binding IgG-containing immune complexes. Hence, the expression level of Fc
Rs on monocytic cells may influence inflammation in patients with rheumatoid arthritis (RA). In this study the expression levels of Fc
RI, 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, Fc
R 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 Fc
R 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 Fc
RIIa and high percentages of Fc
RIIIa-expressing monocytes were found in RA patients with a high erythrocyte sedimentation rate. DMARD-naive early RA patients had higher Fc
RIIa expression levels but a similar amount of Fc
RIIIa-positive monocytes compared with RA patients using DMARDs. In synovial fluid, Fc
RIIa expression levels were lower than in RA peripheral blood, whereas the percentage of Fc
RIIIa-positive monocytic cells was higher in synovial fluid than in peripheral blood.
Conclusions. These data point to the involvement of Fc
Rs, specifically Fc
RIIa and IIIa, in the immune response of RA and suggest that Fc
R expression levels are susceptible to modulation by DMARD therapy.
KEY WORDS: Fc
Receptor, Rheumatoid arthritis, Monocytes/macrophages, DMARDs.
Correspondence to: S. Wijngaarden, Rheumatology and Clinical Immunology (F02.127), University Medical Center Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. E-mail: s.wijngaarden{at}azu.nl
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
A. Kastbom, A. Ahmadi, P. Soderkvist, and T. Skogh The 158V polymorphism of Fc gamma receptor type IIIA in early rheumatoid arthritis: increased susceptibility and severity in male patients (the Swedish TIRA project) Rheumatology, October 1, 2005; 44(10): 1294 - 1298. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Wijngaarden, J. A. G. van Roon, J. G. J. van de Winkel, J. W. J. Bijlsma, and F. P. J. G. Lafeber Down-regulation of activating Fc{gamma} receptors on monocytes of patients with rheumatoid arthritis upon methotrexate treatment Rheumatology, June 1, 2005; 44(6): 729 - 734. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. L. Hepburn, J. C. Mason, and K. A. Davies Expression of Fc{gamma} and complement receptors on peripheral blood monocytes in systemic lupus erythematosus and rheumatoid arthritis Rheumatology, May 1, 2004; 43(5): 547 - 554. [Abstract] [Full Text] [PDF] |
||||
