DEFECTIVE RETICULOENDOTHELIAL SYSTEM FC-RECEPTOR FUNCTION IN SYSTEMIC LUPUS-ERYTHEMATOSUS

To determine whether reticuloendothelial-system immunospecific Fc-receptor function is abnormal in patients with systemic lupus erythematosus, we studied the clearance of IgG-sensitized, 51Cr-labeled erythrocytes by these splenic macrophage membrane receptors in 15 untreated patients. Fc-specific clearance rates were strikingly abnormal in 13 of 15 patients (half-times ranging from 80 to 2256 minutes, P<0.001 as compared to controls). Abnormal clearances correlated with immune-complex levels (as measured by the C1q-binding assay) and with disease activity. C1q-binding activity and anti-DNA titers also correlated with disease activity. The correlations of C3, C4, CH50 and factor B with abnormal clearance and disease activity were weaker or nonexistent. The significant correlations among clearance, disease activity and C1q-binding activity suggest that the defect in Fc-receptor function may lead to the prolonged circulation of immune complexes, thereby contributing to tissue deposition and damage. (N Engl J Med 300:518–523, 1979) IN systemic lupus erythematosus, circulating immune complexes are present in patients with active disease, and it is believed that the activation of complement and other mediators of inflammation by these complexes, and their organ deposition, leads to tissue damage. In support of this concept, immune complexes as well as complement proteins have been demonstrated in various organs undergoing immunologic injury in patients with systemic lupus erythematosus.1 Moreover, complexes have been demonstrated in the serum of patients with active disease.2 However, the factors that govern the fate of immune complexes in the circulation in man and regulate their subsequent tissue deposition. © 1979, Massachusetts Medical Society. All rights reserved.