Rheumatology Advance Access originally published online on January 27, 2004
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Rheumatology 2004; 43: 547-554
Rheumatology Vol. 43 No. 5 (c) British Society for Rheumatology 2004; all rights reserved
Basic Science |
Expression of Fc
and complement receptors on peripheral blood monocytes in systemic lupus erythematosus and rheumatoid arthritis
Rheumatology Section and 1BHF Cardiovascular Medicine Unit, The Eric Bywaters Centre, Imperial College London, Hammersmith Hospital, London and 2Brighton Sussex Medical School, Brighton, UK.
Correspondence to: A. L. Hepburn, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK. E-mail: a.hepburn{at}imperial.ac.uk
Objectives. Fca
and complement receptors play an important role in the interaction between immune complexes (IC) and monocytes/macrophages. Recent work has demonstrated that their relative expression on these cells may be modified by cytokines, including TNF-
and IL-4. Furthermore, cytokines may alter the expression of adhesion molecules such as ICAM-1. However, little data exist on the in vivo expression of specific Fc and complement receptors in systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA), two diseases in which IC are important in pathogenesis.
Methods. Venous blood was obtained from 30 patients with SLE, 25 with RA and 25 healthy controls. Monocyte phenotype was determined by flow cytometric analysis of whole blood samples, with selective gating using forward and side scatter signals. Surface expression of Fc receptors RI (CD64), RII (CD32) and RIII (CD16), complement receptors CR1 (CD35) and CR3 (CD11b/CD18), and adhesion molecules ICAM-1 (CD54) and CD11a (LFA-1) was determined. The effects of disease activity and corticosteroid therapy on the expression of these molecules were also examined.
Results. The expression of FcRII was reduced on monocytes from patients with SLE compared with healthy controls and patients with RA (P = 0.002). This did not correlate with disease activity using conventional indices [SLEDAI (SLE disease activity index), C3/C4 levels and anti-double-stranded DNA antibody titres], and was independent of prednisolone therapy. There was no significant difference in FcRI or RIII expression on SLE monocytes compared with healthy controls. In contrast, the expression of FcRIII was increased on RA monocytes (P = 0.01), this being highest in patients with active disease. The proportion of FcRIII-positive monocytes was also increased in RA, and prednisolone therapy was associated with a lower proportion of FcRIII-positive cells. An increase in CR3 expression was seen on RA monocytes (P = 0.002), whilst CR1 was increased on monocytes from patients with active SLE or active RA. ICAM-1 expression was reduced on monocytes from patients with SLE (P = 0.002), although high-dose prednisolone therapy was associated with the lowest level of surface ICAM-1 on monocytes.
Conclusions. Peripheral blood monocytes from patients with SLE or RA display significantly altered phenotypes compared with those from healthy controls. The observed reduction in SLE of FcRII may represent a mechanism by which monocytes are protected from IC-mediated activation. Prednisolone therapy and disease activity had little effect on phagocytic receptor expression. The observed changes may reflect the different cytokine profiles seen in SLE and RA.
KEY WORDS: Monocyte, Fc receptor, Complement receptor, Rheumatoid arthritis, SLE.
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