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Sixty six patients with systemic lupus erythematosus (SLE) were genotyped using aHindIII restriction fragment length polymorphism identified by CR1.1 cDNA, then were followed up for an average of 50 months to evaluate the stability of their CR1 activities. The gene frequencies for the two alleles which correlate with the numeric expression of CR1 on the erythrocytes were not significantly different between 66 patients with SLE and 52 normal controls. A discrepancy between homozygosity for a high allele and a negative CR1 activity was found in many patients. These patients, however, had significantly lower concentrations ofserum complement than did patients with a positive CR1, and some were in an active state of the disease. Furthermore, there were several patients in whom the CR1 activities changed from negative to positive together with an increase in serum complement. Our results suggest that the decreased expression of CR1 on erythrocytes in patients with SLE is not inherited, rather it is a consequence of the disease processes.

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