Immunomodulation Mechanisms following Transfusion of Allogeneic und Autologous Erythrocyte Concentrates

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Abstract
The residual risk of transmitting a transfusion-associated infectious disease has been considerably reduced in recent years due to improved test procedures and careful donor selection. The mortality associated with transfusion today is caused mainly by hemolytic reactions and the consequences of bacterial contamination of blood components. In addition, the effects of immunomodulation following allogeneic transfusion are not to be overlooked. Donor leukocytes, or their major histocompatibility- complex (MHC) molecules, contained in blood components stimulate above all humoral immune responses (Th2 response) in the recipient, which also causes downregulation of cellular immune responses (Th1 response). Besides the absolute leukocyte count, the length of storage of blood components, which causes a progressive apoptosis, necrosis, and secondary necrosis of leukocytes, appears to be of decisive importance. Stimulation of Th2 immune responses and suppression of Th1 immune responses results from the particular antigen presentation as is encountered for transfusions, and appears to have a causal relation to the higher incidence of postoperative infection observed in recipients of allogeneic transfusions. Contrary to the effects of allogeneic transfusions described in numerous studies, immunological responses following autologous transfusion have hardly been studied to date. Future studies will have to determine whether autologous transfusions cause not only a lack of immunosuppression but also immunostimulation.

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