Avoidance by host tissues of attack by autologous complement proteins is dependent in part on the activities of membrane regulatory factors. One molecule involved in this control is a 70 kD glycoprotein termed decay-accelerating factor (DAF), or CD55. Interruption by CD55 of the complement sequence at an early step in activation effectively halts progression of the cascade and prevents consequent cell injury. In man, CD55 is expressed on the plasma membrane of all cell types that are in intimate contact with plasma complement proteins.