Acute antibody-mediated rejection (AMR), also known as acute humoral rejection, is caused by donor-specific antibodies (DSAs) that bind to endothelial cells, activating complement. The histological features described (microvascular inflammation, neutrophil infiltration, endothelial injury) are consistent with AMR. C4d, a stable degradation product of C4 (part of the classical complement pathway), is deposited on endothelial cells and is a key diagnostic marker for AMR, particularly in peritubular capillaries in kidney transplants, but also seen in other organs like the liver. CD3 is a T-cell marker, relevant for cellular rejection. Alpha-smooth muscle actin is a marker for myofibroblasts, and Cytokeratin 7 is an epithelial marker, neither specific for AMR.
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