INHIBITORS OF COMPLEMENT DERIVED FROM THE ERYTHROCYTE-MEMBRANE IN PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA
- 1 January 1980
- journal article
- research article
- Vol. 55 (5) , 772-776
Abstract
Extracts of membranes of normal [human] red cells and red cells from all subpopulations of paroxysmal nocturnal (PNH) red cells inhibited antibody-mediated complement activation. These extracts accelerated decay of the complement [C] complex, C42, and the relative amount of inhibitory activity was similar in normal and PNH membranes. Inhibitors derived from normal red cells markedly decreased lysis of both PNH and normal cells when antibody was present in excess and C was limiting. These same inhibitors decreased PNH cell lysis to a much lesser degree when C was activated with cobra venom or acidified serum. Susceptibility of the PNH cell to C lysis because of an increased fixation of C3 to its membrane was not due to a difference in membrane-associated accelerator of decay of the C42 complex.This publication has 3 references indexed in Scilit:
- Immune lysis of normal human and paroxysmal nocturnal hemoglobinuria (PNH) red blood cells. I. The sensitivity of PNH red cells to lysis by complement and specific antibody.Journal of Clinical Investigation, 1966
- THE REACTION MECHANISM OF ß1C-GLOBULIN (C'3) IN IMMUNE HEMOLYSISThe Journal of Experimental Medicine, 1966
- STUDIES ON TERMINAL STEPS OF IMMUNE HEMOLYSIS .2. RESOLUTION OF E] TRANSFORMATION REACTION INTO MULTIPLE STEPS1965