Protection of Paroxysmal Nocturnal Hemoglobinuria Erythrocytes by Transferring of GPI-Anchored Protein CD59 from Vesicles of Erythrocytes In Vitro

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic disease characterized by sensitivity of erythrocytes to complement owing to deficiency of glycosylphosphatidylinositol (GPI)- anchored complement regulatory proteins, such as CD55 and CD59. Vesicles released from normal erythrocytes under storage or ATP depleted, are rich in CD59. PNH CD59- cells wwere separated by immuno-affinity column bound with monoclonal antibody CD59, and then incubated with normal erythrocyte vesicles. The content of CD59 and hemolysis of PNH CD59- cells were detected by flow cytometric analysis and cobra venom factor hemolytic test respectively. The fluorescence intensity of PNH CD59- cells was increased and the hemolysis was sighnificantly decreased. It seems that CD59 protein molecules might transfer from normal erythrocyte vesicles to PNH CD59- cells and retain the complement regulatory function. CD59-erythrocytes could be rendered less liable to hemolyze during complement attack.