Colvin Robert B, Smith R Neal
Department of Pathology, Warren 225, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02140, USA.
Nat Rev Immunol. 2005 Oct;5(10):807-17. doi: 10.1038/nri1702.
Recent studies show that alloantibodies mediate a substantial proportion of graft-rejection episodes, contributing to both early and late graft loss. Rejection that is caused by antibody is mediated by different mechanisms from rejection that is caused by T cells, thereby requiring other approaches to treatment and prevention. Antibody induces rejection acutely through the fixation of complement, resulting in tissue injury and coagulation. In addition, complement activation recruits macrophages and neutrophils, causing additional endothelial injury. Antibody and complement also induce gene expression by endothelial cells, which is thought to remodel arteries and basement membranes, leading to fixed and irreversible anatomical lesions that permanently compromise graft function.
近期研究表明，同种异体抗体介导了相当一部分的移植排斥反应，导致早期和晚期移植失败。抗体引起的排斥反应与T细胞引起的排斥反应机制不同，因此需要其他治疗和预防方法。抗体通过补体固定急性诱导排斥反应，导致组织损伤和凝血。此外，补体激活募集巨噬细胞和中性粒细胞，导致额外的内皮损伤。抗体和补体还可诱导内皮细胞的基因表达，这被认为会重塑动脉和基底膜，导致固定且不可逆的解剖学病变，永久性损害移植功能。
