Immune complex clearance by complement receptor type 1 in SLE

Patients with systemic lupus erythematosus (SLE) have relative deficiencies of the C3b/C4b receptor (CR1, CD35) on erythrocytes (E). This receptor takes part in the binding, transport and endocytosis of circulating immune complex bound complement components (ICC). Besides the autoantibodies the abnormalities in IC elimination are fundamental to the pathogenesis of SLE. During the last 15 years more than 100 patients with SLE have been treated in our Department and their data on ICC clearance by ECR1 analyzed. After plasmapheresis the ECR1 expression and also the binding sites for ICC were increased, while the level of IC and autoantibodies were reduced. Stimulating erythropoiesis in patients with anaemia and lupus nephritis caused the decreased expression and functional activity of ECR1 to be improved. In patients with SLE the level of soluble CR1 was also decreased, but a significant portion of soluble CR1 bound ICC in vivo, especially in those with severe renal lesion.