Mononuclear phagocytes in rheumatoid arthritis: Fc-receptor expression by peripheral blood monocytes.

Blood Monocytes in Rheumatoid Arthritis Are Highly Adherent to Cultured Endothelium

“…their surface charge, it seems likely that the increased ad hesiveness of R A monocytes arises from their state of acti vation. That blood monocytes are activated in RA is in ac cord with previous studies which demonstrated that rheu matoid monocytes possess enhanced functional and biochemical activities [9][10][11][12][13][14][15]. Moreover, from the finding that rheumatoid monocytes also express increased surface proteolytic activity [33] it seems that they may directly con tribute to cartilage and connective tissue degeneration in this disease.…”

“…Further support for this view stems from the findings that the num ber of macrophages in RA synovium directly relates to the degree of radiological deterioration [4], and that suppres sion of disease activity by gold treatment is associated with a decrease in the number of synovial macrophages [5], Within chronic inflammatory lesions macrophage prolifer ation is dependent upon the continuous recruitment of blood monocytes [6], and in the rheumatoid synovium, macro phages account for approximately 25-50% of leucocyte in filtrates [7,8], Circulating monocytes in RA exhibit in creased phagocytosis [9], Fc receptor expression [10], chemotaxis [11], and secrete high levels of neopterin ] 12]. The cells also demonstrate enhanced superoxide dismutase ac tivity [13], superoxide anion production [14], and spontane ously release IL-1 [15].…”

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.…”

Studies of the effect of D-penicillamine and sodium aurothiomalate therapy on superoxide anion production by monocytes from patients with rheumatoid arthritis: evidence for in vivo stimulation of monocytes.

“…The mechanisms by which penicillamine and AuTM might be acting (directly or indirectly) include enhancement of monocyte membrane receptor expression, enhancement of the biochemical mechanisms linking receptors to the membrane superoxide generating system, or a combination of both. Previous workers have shown increased monocyte Fc receptor (FcR) expression and increased antibody-dependent cell cytotoxicity in a vanet4 of chronic inflammatory diseases including RA, 26 and this may reflect enhancement of subclasses of FcR which mediate respiratory burst activity.27 28 Increased FcR expression and oxygen free radical release are manifestations of phagocyte activation and occur in response to a variety of chronic inflammatory stimuli.29 Thus one interpretation of our data is that second-line agents act by enhancing mechanisms of phagocyte activation in patients in whom these mechanisms have been impaired. Paradoxically, impairment of the superoxide generating system might occur during chronic inflammation as a consequence of free radical release by phagocytes.…”