Monocyte fc receptor function in rheumatoid arthritis. enhanced cell‐binding of igg induced by rheumatoid factors

Abstract

Monocytes from 11 patients with rheumatoid arthritis and 10 control subjects were purified by countercurrent elutriation. Rheumatoid arthritis monocytes had more cell-associated IgG ( P < 0.001) and bound more 1251-labeled heat-aggregated IgG in vitro (P < 0.02) than did monocytes from control subjects.

Up-regulation of CD64-expressing monocytes with impaired FcγR function reflects disease activity in polyarticular psoriatic arthritis

“…By up-regulating CD64 and binding more IgG, monocytes increase their ability to bind ICs (40). Similar observations have previously been made in RA (41).…”

Uptake and degradation of soluble aggregates of IgG by monocytes of patients with rheumatoid arthritis: relation to disease activity.

“…[17][18][19] In our study we found that monocytes from patients with RA bound significantly more IgG at 4°C, which reflects the number of Fc receptors. The increased binding of '25I labelled IgG aggregates to monocytes of patients with RA compared with that to control monocytes might also be due to the presence of cell bound rheumatoid factor.…”

Modulation of monocyte activation in patients with rheumatoid arthritis by leukapheresis therapy.

“…One of the patients analyzed suffered from severe erosive RA, but had no detectable rheumatoid factors or immune complexes (Clq binding and polyethylene glycol precipitation assay). Thus, at least in this patient it appears unlikely that these humoral factors are by themselves responsible for monocyte activation, which otherwise has been well substantiated (6). In a regular activation pathway, e.g., in infectious disease situations (45,46), monocytes receive their stimulatory signals from T cells.…”

“…There were striking differences between these two monocyte populations. Cells obtained from the first leukapheresis constitutively released large amounts of prostaglandin E2 (PGE2), neopterin, interleukin 1,6 (IL-1I#) and tumor necrosis factor-a (TNF-a). In particular, IL-1jB and neopterin production were further enhanced by stimulation with either interferon-'y (IFN-"y) or TNF-a without a synergistic effect.…”

“…Furthermore, an increased phagocytic activity of monocytes has been demonstrated (4). Possible factors leading to monocyte/ macrophage activation are immune complexes, notably those containing rheumatoid factors (5,6), but also several major cytokines have been implicated in the pathogenesis of rheumatoid arthritis such as interferon-y (IFN--y), tumor necrosis factor-a (TNF-a), and colony-stimulating factors (7,8).…”