“…Two mechanisms which lead to the development of the syndrome are distinguished as refl ected in the following classifi cation: -immune-mediated TRALI, predominantly caused by anti-HLA (human leukocyte antigen) antibodies class I, II and/or less frequent antibodies directed against specifi c antigens of granulocytes -HNA (human neutrophil antigen), present in the serum of the recipient or donor, which react with the donor's or recipient's leukocytes respectively [4,5,7,[12][13][14][15]. -non-immune-mediated TRALI, which may be attributed to transfusion of biologically active compounds accumulated in stored blood components such as bioactive lipids, proinfl ammatory cytokines or platelet microparticles with high procoagulant activity.…”