Abstract
Human erythrocytes (E) have surface receptors for the third component of complement (C3b-IA receptors) which mediate immune adherence haemagglutination (IAHA). We have observed that E from patients with systemic lupus erythematosus had imparied or defective C3b receptor (C3b-R) activity when circulating immune complexes (CIC) were found in serum. This phenomenon has been investigated by a newly developed method involving competitive inhibition of IAHA in patients with immune complex diseases. IAHA involving sheep E coated with antibody and complement (EAC), and indicator human E was inhibited by lysates of E with normal C3b-R activity from healthy donors and a monkey. In contrast, the lysates of E from 95% of patients bearing CIC did not inhibit IAHA, which indicated such E had defective or impaired C3b-R activity. This phenomenon was supported by control studies in which IAHA was not inhibited by lysates of E with absent, inactivated or occupied C3b-R. In those patients, in whom CIC disappeared during immunosuppressive therapy, C3b-R activity slowly returned to normal levels. Moreover, it was observed that C3b-R activity of patients' E decreased with the reappearance of CIC during exacerbations of disease. These observations suggest that CIC are carried in vivo by the C3b-R of E as well as those of the mononuclear phagocyte system, and that the E C3b-R may also contribute to the clearance of CIC.
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