Abstract
Patients with systemic lupus erythematosus (SLE), an autoimmune disease caused by excessive amounts of immune complex in the serum, have a loss of complement receptor type 1 (CR1), a receptor of complements C3b and C4b, on glomerular epithelial cells. In order to calrify the biological function of CR1 on renal glomeruli and the correlation with clearance of immune complex, a full length of human tonsil CR1 cDNA was transfected to normal rat glomerular epithelial cells (SGE1) to enable CR1 expression in the long term (more than 1 year). As compared with the non-CR1-expressing cells, the CR1-expressing cells showed a higher binding effect to immune complex in 60 min, and the binding effect was mediated by complement. Blocking of the binding effect by anti-CR1 antibody indicates that CR1 plays an important role in removal of immune complex. Results from microscopy showing that the constructed cell has an enhanced phagocytic ability in the presence of complement suggest that the mechanism of removing immune complex by CR1-expressing cells has three steps: opsonization of immune complex by complement, the ligand-receptor interaction between opsonized complex and CR1 on the cell, and phagocytosis of complex by CR1-expressing cells.
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