Authors:
JG Wilson, WD Ratnoff, PH Schur, DT Fearon
Journal name: 
Arthritis Rheum
Citation info: 
29(6):739-747
Abstract: 
Decreased numbers of complement receptor type 1 (CR1) have been observed on erythrocytes of patients with systemic lupus erythematosus (SLE) and on glomerular podocytes of patients having proliferative nephritis of SLE. In the present study, the analysis of the cellular expression of CR1 has been extended to include leukocytes. In addition, expression by B lymphocytes of the C3d receptor (CR2), which also serves as the receptor for the Epstein-Barr virus, was assessed. Receptor expression was measured by 2-color fluorescent flow cytometry of peripheral blood B cells, identified by the presence of the B1 antigen, that had also been stained with anti-CR1 or anti-CR2. B cells from 17 patients with SLE exhibited a mean relative fluorescence for CR1 that was 61% of that found in 17 normal individuals (P less than 0.001). The expression of CR2 by the patients' B cells (n = 14) was 62% of that of the B cells from normal subjects (n = 17) (P less than 0.001). The expression of CR1 correlated with that of CR2 among patients (r = 0.63; P less than 0.01) but not with the expression of CR2 among normal individuals (r = 0.36; P greater than 0.1). The mean CR1 content of the patients' neutrophils was only 59% of the normal mean (P less than 0.001). Thus, abnormalities of complement receptor expression occur on the leukocytes of patients with SLE. These deficiencies may be secondary to interaction of the cells with the products of complement activation, or, in some individuals, the deficiencies may be familial.
DOI: 
http://doi.org/10.1002/art.1780290606
E-pub date: 
01 Jun 1986
Users with this publication listed: 
Doug Fearon