作者: Adrianne I. Enos , Pamela S. Hair , Neel K. Krishna , Kenji M. Cunnion
DOI: 10.1016/J.MOLIMM.2020.05.008
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摘要: Abstract Background Platelet refractoriness remains a challenging clinical dilemma although significant advancements have been made in identifying human leukocyte antigen (HLA) matched or HLA compatible units. Antiplatelet antibodies are the major risk factor for immune-mediated platelet refractoriness, yet role of antibody-initiated complement-mediated destruction poorly understood. Study Design and Methods Human opsonization killing platelets was assayed ex vivo using antibody-sensitized incubated with complement-sufficient sera. A new animal model utilizing Wistar rats transfused is described. Results sensitized anti-platelet were rapidly opsonized iC3b upon incubation This could be completely blocked classical pathway complement inhibitor, PA-dPEG24. Complement activation decreased viability, which also reversible inhibitor rat developed that demonstrated some removal from blood stream mediated. Conclusions initiated by leads to viability. adds tool elucidating mechanisms refractoriness.