Abstract
Recent clinical and experimental evidence indicates that many of the sequelae of hemolytic transfusion reactions may be mediated by cytokines, including interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, the chemokines interleukin-8 and monocyte chemoattractant protein-1, and interleukin-1 receptor antagonist. Experimental models of both acute and delayed hemolytic transfusion reactions demonstrate the production of these molecules. The time course and relative patterns of production correlate well with known clinical manifestations of these reactions. Tumor necrosis factor-alpha appears to be central to ABO incompatibility reactions, and stimulates endothelial cells to exhibit procoagulant activity and surface adhesion molecules.
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