Intravenous and standard immune serum globulin preparations interfere with uptake of 125I-C3 onto sensitized erythrocytes and inhibit hemolytic complement activity.
Antibody-sensitized sheep erythrocytes were used as a model to determine the effects of therapeutic immune serum globulin (ISG) preparations on the ability of this particulate activator to fix C3 and initiate hemolysis. Both standard and intravenous forms of ISG inhibit uptake of 125I-C3, presumably by competing for the deposition of "nascent" C3b molecules onto the erythrocytes. Both forms of ISG also inhibit hemolytic activity of whole serum or purified complement components. The inhibition appears to be a specific property of IgG itself, since similar inhibition was not caused by equivalent concentrations of human serum albumin, and was not affected by the buffer in which the ISG was dissolved. Interference with C3 uptake onto antibody-sensitized platelets and/or inhibition of hemolytic complement activity could contribute to the efficacy of high dose intravenous ISG in idiopathic thrombocytopenic purpura.
D003167:Complement Activation; D003176:Complement C3 / Q000378:metabolism*; D003171:Complement Pathway, Classical; D004912:Erythrocytes / Q000276:immunology; D006461:Hemolysis / Q000187:drug effects*; D006801:Humans; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D007275:Injections, Intravenous; D007457:Iodine Radioisotopes; D011696:Purpura, Thrombocytopenic / Q000628:therapy
D003176:Complement C3; D007074:Immunoglobulin G; D007457:Iodine Radioisotopes