Alloantibodies cause acute rejection by binding to alloan-tigens, mainly HLA molecules, on vascular endothelial cells, causing endothelial injury and intravascular thrombosis that results in graft destruction (see Fig. 16-8B). The binding of the alloantibodies to the endothelial cell surface triggers local complement activation, which leads to lysis of the cells, recruitment and activation of neutro-phils, and thrombus formation. In addition, alloantibody binding to the endothelial surface may directly alter endothelial function by inducing intracellular signals that enhance surface expression of proinflammatory and procoagulant molecules.
The histologic hallmark of this form of acute rejection is transmural necrosis of graft vessel walls with acute inflammation (Fig. 16-9C), which is different from the thrombotic occlusion without vessel wall necrosis seen in hyperacute rejection. Immunohistochemical identification of the C4d complement fragment in capillaries of renal allografts is used clinically as an indicator of activation of the classical complement pathway and humoral rejection (Fig. 16-9D). In a significant fraction of cases of antibody-mediated rejection, there is no C4d deposition detectable, suggesting that damage is caused by the complement-independent effects of alloantibody binding to endothelial cells, mentioned before.
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