Changes in the phenotype of monocytes/macrophages and expression of cytokine mRNA in peripheral blood and synovial fluid of patients with rheumatoid arthritis

Abstract

SUMMARY Data from a previous study suggested that peripheral blood monocytes in patients with rheumatoid arthritis (RA) may be activated. Therefore, in this study we sought further evidence of ‘presynovial’ activation of monocytes. Our results show that phenotypic changes are demonstrable in peripheral blood monocytes in patients with RA, including increased expression of CR3 (CDllb/CD18) and FcRI (CD64). However, changes are most extensive in synovial monocytes/macrophages and especially for HLA‐DR and intercellular adhesion molecule‐1 (ICAM‐1) (CD54). We conclude that monocyte/macrophage activation is most evident within the joint, and that ‘presynovial’ changes occur but are of limited extent.

Fcγ receptor profile of monocytes and macrophages from rheumatoid arthritis patients and their response to immune complexes formed with autoantibodies to citrullinated proteins

“…Such an increase was also reported in two studies,33 34 but not in two other studies,35 36 and contrasts with the decrease reported in two additional studies 37 38. Our observation that the percentages of FcγRI-positive cells are more heterogeneous and significantly decreased in RA patients compared with HC is unique, and was not reported in the above-mentioned works.…”

Activation of human synovial mast cells from rheumatoid arthritis or osteoarthritis patients in response to aggregated IgG through Fcγ receptor I and Fcγ receptor II

“…Using immunohistochemistry, Blom et al demonstrated that the expression of Fc␥RII and Fc␥RIII on tissue macrophages from patients with RA was higher than that on tissue macrophages from healthy control subjects; however, the Fc␥RI expression levels were comparable (39). The Fc␥RI expression level is reportedly higher on peripheral blood and synovial fluid monocytes from patients with RA than on monocytes from normal subjects or patients with OA or reactive arthritis (40,41). The expression levels of C5a receptor (CD88) on synovial MCs from patients with RA are reportedly higher than those on synovial MCs from patients with OA (23).…”

The functional variant of the inhibitory Fcγ receptor IIb (CD32B) is associated with the rate of radiologic joint damage and dendritic cell function in rheumatoid arthritis

“…In humans, various investigators have focused on the expression levels of activating and inhibiting FcγRs on various cell types. Highton et al demonstrated that the expression of FcγRI is increased on circulating monocytes from RA patients (13). These findings were corroborated by Shinohara and colleagues, who found an increased expression of FcγRI and FcγRII in RA patients with active disease as well as in those with disease in remission (14), an observation that was later confirmed by 2 other research groups (15–17).…”