Monocytes from patients with
rheumatoid arthritis (RA) and
rheumatoid vasculitis have a diminished ability to degrade soluble complexes of aggregated
IgG in the absence (mediated by
Fc receptors) as well as in the presence of
complement (C) (mediated by (Fc + C) receptors). To investigate whether a relation exists between the receptor mediated degradation of aggregated
IgG by adherent monocytes and disease activity a longitudinal study was performed in 79 patients with RA and
rheumatoid vasculitis over a period of 16 months. Adherent monocytes were incubated in vitro with 125I labelled
IgG aggregates of restricted size in the absence or presence of fresh serum and the percentage of catabolised
IgG aggregates was measured. Cross sectionally the degradation of aggregated
IgG by monocytes, mediated by Fc and (Fc + C) receptors, correlated significantly with disease activity as scored by the Ritchie articular index, the presence of extra-articular features, and circulating
immune complexes. A high number of
Fc receptors on monocytes correlated with diminished degradation, whereas high numbers of
complement receptors 1 and 3 correlated with enhanced degradation of aggregated
IgG mediated by both Fc and (Fc + C) receptors. The degradation of aggregated
IgG by monocytes did not correlate with disease activity in individual patients followed up longitudinally. When patient groups were formed according to the results of longitudinal studies, however, degradation of aggregated
IgG mediated by Fc and (Fc + C) receptors was significantly decreased in patients with
rheumatoid vasculitis and in patients with active RA in comparison with patients with inactive RA and healthy controls. Patients with active RA and
rheumatoid vasculitis also expressed significantly more
Fc receptors and less
complement receptors on the monocytes than patients with inactive RA.
Drug treatment did not correlate with receptor expression or the degradation of aggregated
IgG by monocytes either in cross sectional or longitudinal studies. It is concluded that in RA disease activity is related to receptor expression and the degradation of soluble immune aggregates by monocytes.