Characterization of immune complexes and immunoglobulin G antibodies reactive with neutrophils in the sera of patients with Felty's syndrome.
These studies were performed to determine the relative contribution of immune complexes or antibodies reactive with PMNs to the elevated levels of IgG PMN-binding activity seen with sera from some patients with Felty's syndrome. Twenty-one sera from 19 patients with Felty's syndrome were fractionated by gel filtration on Sephadex G-200. Fourteen of the sera had elevated levels of IgG PMN-binding activity as measured by a sensitive IgG-specific antiglobulin inhibition technique. Ten of the G-200 excluded pools and eight of the G-200 IgG pools had levels of IgG PMN-binding activity greater than 2 S.D. above the mean value for normals.Significant correlations were observed between the levels of IgG PMN-binding activity in the sera and the values for both the G-200 excluded pools (r = 0.51) and the IgG pools (r = 0.69). These data suggested that both soluble immune complexes and antibodies reactive with PMNs contributed to the elevated serum levels of IgG PMN-binding activity seen with sera from some patients with Felty's syndrome. Further evidence for the presence of PMN-binding immune complexes in the sera of patients with Felty's syndrome was the strong correlation between the values of serum IgG PMN-binding activity and the levels of immune complexes as detected by C1q binding (r = 0.71) or analytical ultracentrifugation (r = 0.60). Studies of G-200 excluded samples adsorbed with human IgG coupled to Sepharose 4-B indicated that immune complexes containing rheumatoid factors contributed only in part to the increased levels of IgG PMN-binding activity and of C1q-binding activity. Confirmation of the presence of antibodies reactive with neutrophils was the finding of significantly greater binding to PMN with F(ab')2 fragments of IgG from four sera of patients with Felty's syndrome compared to F(ab')2 from normal sera. Adsorption studies suggested that the PMN-reactive antibodies did not possess rheumatoid factor activity.
D000327:Adsorption; D000906:Antibodies / Q000032:analysis*; D000936:Antigen-Antibody Complex; D003165:Complement System Proteins / Q000276:immunology; D005258:Felty Syndrome / Q000097:blood* / Q000276:immunology; D006801:Humans; D007106:Immune Sera / Q000276:immunology; D007074:Immunoglobulin G / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D010434:Pepsin A / Q000276:immunology; D012216:Rheumatic Diseases / Q000276:immunology; D012217:Rheumatoid Factor / Q000276:immunology; D014461:Ultracentrifugation
D000906:Antibodies; D000936:Antigen-Antibody Complex; D007106:Immune Sera; D007074:Immunoglobulin G; D003165:Complement System Proteins; D012217:Rheumatoid Factor; D010434:Pepsin A