No quantitative relationship between CR1 and lutheran expression on erythrocytes: In(Lu) gene product is not a common regulator of CR1 expression on erythrocytes

The density of CR1, the C3b/C4b receptor (CD35), on erythrocytes (E) (CR1/E ) is genetically determined. However, the broad distribution of CR1/E withi n a given genotype suggests that other genetic elements might contribute to the regulation of CR1/E. In some pathological conditions, including system ic lupus erythematosus (SLE), AIDS and hemolytic anemia, CR1 deficiency par allels the severity of the disease. When compared to healthy individuals, a n accelerated decrease in CR1/E in these patients has been demonstrated, bu t other mechanisms interfering with CR1 density regulation during erythropo iesis might also contribute. In exceptional circumstances, CR1/E can be dra matically decreased in healthy individuals by the effect of a regulatory ge ne, In(Lu), that switches off various surface molecules on E, the structure genes of which are located on four different chromosomes, suggesting a tra nscription regulatory role for In(Lu) gene products. The hypothesis that pr oducts of this gene could physiologically regulate the surface density of a ll these molecules has been tested by determining Lu-b density on E (Lu-b/E ) using quantitative flow cytometry. Lub antigenic sites were then compared to CR1/E among healthy individuals of the different CR1 density phenotypes , SLE patients with and without CR1 deficiency, and an exceptional SLE pati ent totally lacking CR1/E and reticulocytes. No quantitative relationship w as found between CR1 and Lu-b expression in either normal or pathological c onditions. These data establish that In(Lu) products are not involved in no rmal or pathological CR1 density regulation.