Mononuclear phagocyte system complement receptor dysfunction in rheumatoid arthritis.
To explore the relationship between complement-dependent and Fc receptor-mediated clearance mechanisms, clearance studies were performed in nine patients with definite rheumatoid arthritis and 49 normal controls. Kinetic analysis allowed evaluation of the four rate constants governing both complement- and Fc-mediated clearance processes. This analysis revealed that patients with rheumatoid arthritis had significantly reduced values for the constants regulating complement-dependent clearance (p less than 0.001). Complement-mediated clearance dysfunction was associated with normal serum complement levels and normal Fc receptor function. These data indicate that complement-mediated clearance defects are neither the simple result of a hypocomplementemic complement opsonization deficiency nor merely the reflection of profound Fc dysfunction. Defects in the two clearance processes can occur independently. These data demonstrate a specific complement receptor defect in the fixed tissue macrophages of patients with rheumatoid arthritis.
D000328:Adult; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D003165:Complement System Proteins / Q000276:immunology*; D004912:Erythrocytes / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007518:Isoantibodies / Q000276:immunology; D007700:Kinetics; D010586:Phagocytes / Q000276:immunology*; D011951:Receptors, Complement / Q000172:deficiency*; D011961:Receptors, Fc / Q000276:immunology
D007074:Immunoglobulin G; D007518:Isoantibodies; C033242:RH-antibodies; D011951:Receptors, Complement; D011961:Receptors, Fc; D003165:Complement System Proteins