Antibody-mediated rejection (AMR) after liver transplantation (LT) is increasingly recognized as a cause of graft dysfunction, chronic injury, and graft loss, but remains difficult to diagnose because serologic, histologic, and clinical findings are often incomplete or overlapping. This review focuses specifically on liver AMR and distinguishes liver-specific evidence from mechanisms inferred from experimental models or other solid-organ transplants. We summarize how donor-specific antibodies (DSA), complement activation, Fc receptor-mediated effector mechanisms, endothelial activation, and microvascular inflammation interact with the liver graft’s relative resistance to humoral injury. We also discuss the diagnostic overlap among acute AMR, chronic AMR, T cell-mediated rejection, and plasma cell-rich rejection, and propose a practical diagnostic-therapeutic framework integrating DSA, C4d, histology, graft dysfunction, and mechanism-based treatment options.
Luo et al. (Wed,) studied this question.
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