Low C3B receptor reactivity on erythrocytes from patients with systemic lupus erythematosus detected by immune adherence hemagglutination and radioimmunoassays with monoclonal antibody

Abstract

C3b receptor (CR1) on erythrocytes from 23 patients with systemic lupus erythematosus (SLE) and 124 normal controls was determined by immune adherence hemagglutination (IAHA) and radioimmunoassay. The binding of radiolabeled monoclonal anti‐CR1 to erythrocytes and their lysate was distributed continuously in a wide range. The majority of SLE patients showed low binding by both assays. CR1 sites on erythrocytes were determined also by Scatchard plot analysis and standardized by the number of similarly determined lectin‐binding sites that served as a measure of erythrocyte surface. The numbers of standardized CR1 sites were classified as high, intermediate, and low. Thirty‐six percent of control subjects had high numbers of CR1 sites, 53% had intermediate numbers, and 11% had low numbers. Of SLE patients, the numbers of CR1 sites were high in 0%, medium in 52%, and low in 48%. Negative IAHA was found in 10 controls (8%), all of whom had low numbers of standardized CR1 sites. Among 13 SLE patients with negative IAHA, 11 had low numbers of CR1 sites and the remaining 2 had low intermediate numbers. IAHA, therefore, was particularly efficient in detecting the low numbers of CR1 sites in SLE, which would impair the disposal of circulating immune complexes and accelerate the development of tissue injuries.

Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphocytes and of CR1 on neutrophils of patients with systemic lupus erythematosus

“…The role of genetic factors in SLE in general (54-56) and the observations of familial deficiencies of erythrocyte CRl in this study and in previous studies (1,3,5) led to an analysis of CR1 expression by B cells of the first-degree relatives of 8 patients. Although the mean expression of this receptor by cells from all re1,atives did not differ from that of cells from normal persons, those relatives having low expression of CR1 tended to cluster in families in which more than 1 member had SLE ( Figure 5).…”

“…Three studies have shown that deficiency of erythrocyte CR1 occurs not only in patients with SLE, but also in their relatives (1,3,5). Therefore, we analyzed the CR1 and CR2 of leukocytes obtained from the members of 8 families having a lupus proband.…”

“…In normal individuals, the number of CRl on erythrocytes is genetically regulated (3,5,6). In CR1-deficient SLE patients, both inherited (1,3,5) and acquired (2,6,7) factors, including complement activation (6,7) and autoantibody to the receptor (1 l), have been shown to contribute to the abnormality. A functional consequence of the erythrocyte CR1 deficiency may be the impaired clearance of immune complexes from the intravascular space (12).…”

Complement C3b receptors on erythrocytes in patients with juvenile rheumatoid arthritis

“…The numbers of erythrocyte CR1 in healthy individuals seem to be genetically determined (8,(19)(20)(21)(22). The origin of the reduction in numbers of CRl in patients with SLE has been the subject of discussion.…”

Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE)

“…The erythrocytes (E) of many patients with SLE display a relative deficiency of complement receptor (CRl) [1][2][3][4][5][6][7][8] as well as increased deposition of the C3-split product, C3d,g, on the E-membrane [9][10][11][12]. Both inherited [3,7] and acquired [1,4,6] factors have been reported to contribute to the deficiency of E-CRl in SLE patients.…”