Complement receptor (CR1) deficiency in erythrocytes from patients with systemic lupus erythematosus.

Abstract

Quantitative information is provided on the concentration of receptors for complement components C3b and C4b (CR1) on erythrocytes from normal individuals and patients with immune complex disease. The measurements were performed by an immunoradiometric assay using monoclonal antibodies against CR1. The antibody specificity was confirmed by immunoprecipitation of CR1 from extracts of surface-labeled cells, by inhibition of rosette formation between B lymphocytes and the erythrocyte intermediate erythrocyte-antibody-complement [EAC]14oxy23b and by the characteristic distribution of the antigen among human peripheral blood cells. The number of CR1 molecules in erythrocytes from 52 normal individuals was estimated as 1410 .+-. 620. No significant differences in CR1 levels were observed when individuals were grouped by sex, age or blood groups. In patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis, the number of CR1 molecules per erythrocyte was significantly lower, i.e., 600 .+-. 307 and 903 .+-. 417, respectively. CR1 levels were normal in asthmatics undergoing long-term treatment with prednisone. In SLE patients, significant correlations were found between CR1 levels, C4 hemolytic titers, and levels of circulating immune complexes. In 2 of 4 patients with SLE, CR1 levels increased significantly during remission, showing that the deficiency is, at least in part, reversible. The deficiency in CR1 could be genetically controlled or could represent an epiphenomenon caused by the interaction of the receptor with a ligand present in the circulation of patients.