Transfusion-associated immune modulation: a reason to TRIM platelet transfusions?

摘要

Each blood component is essentially a unique product not only because the donors differ, but because constituent cells, biomolecules, additives, and even container materials interact with each other after collection such that they are fundamentally altered by time and storage.1 This complexity increases the possibility of idiosyncratic adverse events after transfusion and of immunologic reactions in particular. Potentially, 1 to 5 percent of a recipient's T lymphocytes can recognize each allogeneic HLA allele in a ' transfused component. Recipient B lymphocytes can respond to allogeneic molecules within transfused blood. Stored blood further accumulates a menagerie of biologically active compounds: cytokines, activated complement components, and other biologic response mediators that can modulate a recipient's response to transfused blood. Indeed, the most common significant transfusion reactions, including hemolytic, febrile, allergic, and transfusion-related acute lung injury reactions (TRALI), result from immune responses to blood transfusions. We perceive these different reactions only when the causative immune response achieves a clinically perceptible threshold. But every homologous transfusion is an immunologi-cally significant event that may either up regulate or down modulate specific components of the immune system, and does so in ways not currently predictable by us#