Effect of Anti P 1 M Antibody on Human Platelets

We studied the interaction of complement with human platelets. Complement was activated by lgG anti-Pi Al antibody obtained from 3 patients with the post-transfusion purpura syndrome. We used a heparin-plasma buffer system that permits complement activation and also preserves platelet function. With this system complement activation was efficient, and platelet immune alteration was extensive. AntiP1 Al antibody was effective only in the presence of complement, in which case both platelet lysis and serotonin release (release reaction) in the absence of lysis were observed. Platelet lysis. as assessed by 51Cr loss, required 10-fold more antibody than was necessary to induce platelet aggregation and release of 14C-serotonin. This platelet release reaction required an intact classic complement sequence through C6. The extent of platelet serotonin release paralleled the depletion of Cl and C4 from platelet-rich plasma. Concentrations of antibody insufficient to induce platelet aggregation and serotonin release could still activate Cl and deposit increased C3 on the platelet surface. These studies demonstrated that complement activation by anti-Pi Al antibody can alter human platelets in a nonlytic system. Several phases of complement-mediated human platelet alteration are possible. depending on the concentration of antipl antibody.