HLA-antibody-induced platelet alterations are mediated by (a) complement-independent (Heinrich et al, Brit. J. Haematol., 35, 443, 1977) and (b) complement-dependent mechanisms. To prove the latter hypothesis platelet-rich plasma (PRP) of HLA-typed donors was incubated with HLA-specific sera and various inhibitors of platelet function (prostaglandin-E1 (PGE1), acetyl-salicylic acid (ASA), N-ethyl maleimide (NEM), adenosin, 2-desoxy-glucose + antimycin A (2-DOG + ANT.A)), furthermore an inhibitor of complement activation (cobra venom factor (CVF)) and EDTA or heparin known to interfer with platelet function and complement activation. Methods: Platelet aggregation (Born), Hc-seroto-nin release and 51Cr release. Results: Contrary to collagen-and thrombin-induced platelet alteration, PGE1, NEM, ASA, adenosin and 2-DOG+ANT. A exhibited only moderate inhibition of antibody-induced platelet alteration. However, EDTA, heparin and CVF+PGE1 strongly inhibited antibody-induced platelet alteration. The results support the concept of two pathways for specific HLA-antibody action on platelets: (a) a complement-independent mechanism resulting in aggregation and release and (b) a complement dependent, lytic mechanism.
Effect of IVIG administration on complement activation and HLA antibody levels
