Baldwin William M, Ota Hirofumi, Rodriguez E Rene
Department of Pathology, Ross Research Bldg., Room 659, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Springer Semin Immunopathol. 2003 Sep;25(2):181-97. doi: 10.1007/s00281-003-0133-3.
After decades of neglect, complement has been rediscovered as a potent mediator and diagnostic indicator of inflammation and rejection in organ transplants. In part, this reflects a better understanding of the biology of complement, but it also reflects changes in clinical practice. The relevance of complement to clinical transplantation has increased as access to transplantation continues to be extended. Extended criteria for organ donors include older donors and non-heart beating donors. Simultaneously, the criteria for recipients have been extended to include more presensitized and blood group incompatible recipients. All of these variables can increase complement activation. As a result, several components of complement have received attention as potential diagnostic tools, and, with more sophisticated reagents, evidence of complement activation has been found in larger numbers of biopsy samples. Understanding the biology of complement is important to appreciate fully the diagnostic and mechanistic implications of complement activation in organ transplants. Mechanistically, a series of effector molecules in the complement cascade mediate proinflammatory functions that can account for chemotaxis and activation of cells of the innate immune system, such as granulocytes and monocytes. Simultaneously, many of these same complement mediators activate and disrupt the endothelial cell interface between the recipient and the transplant. In addition, there is growing appreciation that complement can stimulate B and T lymphocytes of the adaptive immune system. More recent evidence indicates that complement participates in the non-inflammatory clearance of apoptotic cells. Therefore, the complement cascade can be activated by multiple mechanisms and various components of complement can modulate the response to transplants in different directions.
在被忽视数十年后，补体已被重新发现，成为器官移植中炎症和排斥反应的强效介质及诊断指标。这部分反映了对补体生物学的更深入理解，但也反映了临床实践的变化。随着移植机会的不断增加，补体与临床移植的相关性也在增强。扩大的器官供体标准包括老年供体和非心脏跳动供体。同时，受体标准也已扩大，纳入了更多预先致敏和血型不相容的受体。所有这些变量都会增加补体激活。因此，补体的几个成分作为潜在的诊断工具受到了关注，并且随着试剂的日益精密，在更多活检样本中发现了补体激活的证据。了解补体生物学对于充分认识补体激活在器官移植中的诊断和机制意义至关重要。从机制上讲，补体级联反应中的一系列效应分子介导促炎功能，这些功能可解释先天免疫系统细胞（如粒细胞和单核细胞）的趋化作用和激活。同时，许多相同的补体介质会激活并破坏受体与移植器官之间的内皮细胞界面。此外，人们越来越认识到补体可刺激适应性免疫系统的B淋巴细胞和T淋巴细胞。最近的证据表明，补体参与凋亡细胞的非炎性清除。因此，补体级联反应可通过多种机制激活，补体的各种成分可在不同方向调节对移植器官的反应。
