Decreased Complement Mediated Binding of Antibody/³H‐dsDNA Immune Complexes to the Red Blood Cells of Patients with Systemic Lupus Erythematosus, Rheumatoid Arthritis, and Hematologic Malignancies

Abstract

The complement mediated binding of prepared antib~dy/~H-dsDNA immune complexes to the red blood cells obtained from a number of patient populations has been investigated. Patients with solid tumors have binding activity similar to that seen in a normal group of individuals. However, a significant fraction of patients with systemic lupus erythematosus, rheumatoid arthritis, and hematologic malignancies have lowered binding activity compared with normal subjects. Quantitative studies indicate the lowered activity probably arises due to a decrease in complement receptors on the respective red blood cells. The potential importance and implications of these findings are briefly discussed. It is well established that complement-fixing antibody/dsDNA immune complexes play a key role in the pathogenesis of SLE (17,18). We have previously performed quantitative experiments (5-8) which demonstrate that large, soluble antibody/dsDNA immune complexes bind to the CR, receptors of normal human

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

“…This means that in order for 2 erythrocytes to be connected by C3b-bearing AHG, 2 or more CRl sites located in close proximity to each other on each erythrocyte would be necessary. Recently, Taylor et a1 made a similar observation (22). They produced immune complexes involving macromolecular 3H-double-stranded DNA (3H-dsDNA) and corresponding antibody.…”

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.…”

Increased frequency of the long (S) allotype of CR1 (the C3b/C4b receptor, CD35) in patients with systemic lupus erythematosus

“…Patients with SLE exhibit a defective complement-mediated clearance of immune complexes which is dependent on decreased opsonizing capacity of hypocomplcmcntacmic scrum and on a deficiency in the quantitative expression of CRI on erythrocytes [1,[19][20][21][22]. Decreased expression of CRI on patients' erythrocytes is not due to an overrepresentation of the gene coding for a low number of CRI on erythrocytes, as indicated by studies of the quantitative CRI RFLP [23][24][25][26].…”

“…One of the biological functions of CRI is to mediate the uptake and transport of C3-and C4-bearing immune complexes on erythrocytes in the circulation [3][4][5][6][17][18][19][20]. CRI allotypes differ by the number of expressed binding sites for C3b, with the S allotype carrying five C3b and/or C4b binding sites instead of four in the F allotype and three in the F' allotype [9].…”