Inhibition of C1q binding to antigen-antibody complexes by a factor in rheumatoid arthritis serum.
The sera and synovial fluids of patients with rheumatoid arthritis (RA) contain a factor which decreases the binding of C1q to antigen-antibody complex (IC). Several lines of evidence suggest that this factor is distinct from the documented C1q inhibitor which is a chondroitin sulphate. It binds to IC rather than to C1q. It is resistant to digestion with chondroitinase ABC. The addition of chondroitin sulphate to serum does not inhibit the binding of IC to C1q. The observation that three purified IgM and IgG rheumatoid factors (RF) did not reduce C1q binding to IC indicates that the factor is not RF. The ability of RA sera to reduce IC binding to C1q was inversely correlated with their ability to prevent immune precipitation (PIP), and directly with levels of an inhibitor of PIP. These data suggest that the factor which binds to IC and reduces C1q binding may be responsible for the excessive immune precipitation which occurs in RA sera.
D000936:Antigen-Antibody Complex / Q000378:metabolism*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000276:immunology*; D003166:Complement Activating Enzymes / Q000378:metabolism*; D003167:Complement Activation / Q000187:drug effects; D003172:Complement C1 / Q000378:metabolism*; D015922:Complement C1q; D003169:Complement Inactivator Proteins / Q000276:immunology; D005260:Female; D006801:Humans; D008297:Male; D013582:Synovial Fluid / Q000276:immunology
D000936:Antigen-Antibody Complex; D003172:Complement C1; D003169:Complement Inactivator Proteins; D015922:Complement C1q; D003166:Complement Activating Enzymes