Purpose of review: Hemolytic transfusion reactions (HTRs) are potentially fatal complications of blood transfusions. Many studies, primarily performed in vitro, have provided a great deal of insight into the initiating events of HTRs; however, it is not clear how they are modulated and how they combine to lead to one or more of the final common pathways. Recently developed mouse HTR models now make it possible to enhance our understanding of the pathogenesis of HTRs; this will allow for the rational design of specific therapies to prevent or ameliorate this serious complication in transfusion medicine.
Recent findings: Mouse models support the hypothesis that 'cytokine storm' plays an important role in the pathogenesis of HTRs. Nitric oxide and endothelial cell dysfunction are also implicated in the pathophysiology of these reactions. In addition, the intriguing phenomenon of 'antigen loss,' in which antigen crosslinking by alloantibody leads to antigen removal rather than red blood cell clearance, has been modeled and explored. Finally, these mouse models were used to evaluate new therapeutic targets employing complement receptor 1 peptide homologues and the antimacrophage agent, liposomal clodronate.
Summary: Models of HTRs are valuable for gaining a better understanding of the pathophysiology of these potentially fatal complications of blood transfusion. The participation of various inflammatory mediators was shown to play a role in these reactions in vivo. This knowledge will lead to novel treatment options.