Inhibition of Fc-rosette formation by synovial fluids from patients with rheumatoid arthritis

SUMMARY Human red cells sensitized with one of the Rh antisera (Ripley) form rosettes (Fc-rosette) with human B lymphocytes and the rosettes are well inhibited by aggregated human IgG. As synovial fluids from patients with rheumatoid arthritis are usually hypocomplementaemic and frequently contain immune complexes, they were used for the inhibition of Fc-rosette formations in this study. The Fc-rosette inhibitory rates were inversely correlated with the levels of CH50 and C4 in the synovial fluids. Fractionation studies of the synovial fluids by ultracentrifugation and Sephadex G200 gel filtration indicated that main inhibitory activities were present in macromolecular fractions. Reduction and alkylation of the synovial fluids resulted in marked reductions of inhibitory activities. The tested synovial fluids did not contain anti-HLA activity as assessed by the microcytotoxicity test. The Fc-rosette inhibitory rates were not correlated with the levels of C3 and immunoglobulins, nor with the activity ofrheumatoid factors in the synovial fluids. These results indicate that the Fc-rosette formations are inhibited by the immune complexes contained in the synovial fluids and it was confirmed that the Fc-rosette inhibition test is a simple and sensitive method for the detection of circulating immune complexes. Our previous study showed that human red cells sensitized with one ofthe Rh antisera (Ripley) formed rosettes (Fc-rosette) with some human lymphocytes and these rosettes were well inhibited by hypocom-plementaemic systemic lupus erythematosus sera (Morito et al., 1976). The inhibitions were ascribed to the presence of immune complexes in the sera. However, it is well known that complement levels of synovial fluids from patients with rheumatoid arthritis are usually depressed in spite of their relatively high content of total protein (Pekin and Zvaifler, 1964; Bunch et al., 1974), and that immune complexes are frequently detectable in these synovial fluids (Hannestad, 1967; Winchester et al., 1971