Department of Pathology, The Johns Hopkins University School of Medicine, Ross Bldg. 664B, Baltimore, MD 21205, USA.
Immunol Res. 2010 Jul;47(1-3):25-44. doi: 10.1007/s12026-009-8136-3.
Antibody-mediated rejection has become critical clinically because this form of rejection is usually unresponsive to conventional anti-rejection therapy, and therefore, it has been recognized as a major cause of allograft loss. Our group developed experimental animal models of vascularized organ transplantation to study pathogenesis of antibody- and complement-mediated endothelial cell injury leading to graft rejection. In this review, we discuss mechanisms of antibody-mediated graft rejection resulting from activation of complement by C1q- and MBL (mannose-binding lectin)-dependent pathways and interactions with a variety of effector cells, including macrophages and monocytes through Fcgamma receptors and complement receptors.
抗体介导的排斥反应已成为临床上的一个关键问题,因为这种排斥反应通常对常规的抗排斥治疗无反应,因此,它已被认为是同种异体移植物丢失的主要原因。我们小组建立了血管化器官移植的实验动物模型,以研究导致移植物排斥的抗体和补体介导的内皮细胞损伤的发病机制。在这篇综述中,我们讨论了补体通过 C1q 和 MBL(甘露聚糖结合凝集素)依赖性途径的激活以及与各种效应细胞(包括巨噬细胞和单核细胞)通过 Fcγ 受体和补体受体的相互作用导致抗体介导的移植物排斥的机制。