Structural polymorphisms of complement receptor 1 (CR1) in systemic lupus erythematosus (SLE) patients and normal controls of three ethnic groups

• Published in: Clinical and experimental immunology 1996-08, Vol.105 (2), p.302-305
• Main Authors: MOULDS, J. M., REVEILLE, J. D., ARNETT, F. C.
• Format: Article
• Language: English
• Subjects: Alleles; Biological and medical sciences; Black or African American; Black People - genetics; C3b/C4b receptor; CR1; Humans; Lupus Erythematosus, Systemic - immunology; Medical sciences; Mexican Americans; Molecular Weight; molecular weight polymorphism; Original; Polymorphism, Restriction Fragment Length; Receptors, Complement 3b - chemistry; Receptors, Complement 3b - genetics; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; systemic lupus erythematosus; White People - genetics
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1046/j.1365-2249.1996.d01-748.x

CR1 exhibits a molecular weight polymorphism and variability in the number of C3b‐binding sites. Because this may affect immune complex clearance, we used erythrocytes to investigate the CR1 size polymorphism in SLE patients from three ethnic groups. The CR1‐C allele was found more frequently in African–Americans, but the frequency did not differ between controls (10%, n = 63) and SLE patients (9%, n = 79). A 160‐kD band similar to CR1‐C was noted in a number of patients and was shown to be a proteolytic cleavage fragment. The study shows that the smallest form of CR1, i.e. CR1‐C, is not a genetic risk factor for SLE and that the frequencies of the CR1 structural alleles do not differ from race‐matched healthy controls.