DNA antibodies with and without complement-binding ability.
The relationship between immunoglobulin class and complement-binding ability of DNA antibodies was studied by indirect immunofluorescence and Crithidia luciliae (CL) as substrate in the sera of 28 patients with SLE and antibodies to CL-DNA. In 15 of 28 cases the antibodies bound complement and were IgG either alone or in combination with IgA and IgM. In the remaining 13 sera the antibodies were either IgA or IgM and did not bind complement. Only one of nine patients with nephritis had CL-DNA antibodies of IgM alone, whereas that was true for 10 of 19 patients without nephritis. The factors influencing the complement binding were further studied by using purified IgM rheumatoid factors. Their ability to 'mask' the IgG-type CL-DNA antibodies and to inhibit the binding of complement was confirmed. These findings suggest that complement activation in SLE does not occur in patients with IgM-type anti-ds-antibodies or in patients with rheumatoid factor activity.
D000906:Antibodies / Q000276:immunology*; D003165:Complement System Proteins / Q000378:metabolism*; D003421:Crithidia / Q000276:immunology; D004247:DNA / Q000276:immunology*; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008297:Male; D009393:Nephritis / Q000276:immunology; D012217:Rheumatoid Factor / Q000276:immunology
D000906:Antibodies; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D003165:Complement System Proteins; D004247:DNA; D012217:Rheumatoid Factor