Martinez O M, Krams S M
Department of Surgery, Stanford University School of Medicine, CA 94305, USA.
Int Rev Immunol. 1999;18(5-6):527-46. doi: 10.3109/08830189909088497.
The Fas/Fas ligand (FasL) pathway has been shown to be important in T lymphocyte-mediated cell death and is a key peripheral immunoregulatory mechanism that limits expansion of antigen-activated lymphocytes. The expression of Fas by commonly transplanted organs such as the heart, lung, kidney, and liver suggests that these tissues may be targets of FasL-expressing allospecific cytotoxic T lymphocytes. In this review the current literature examining the Fas/FasL system as a potential cellular effector pathway in tissue injury is discussed. In addition to a deleterious role in destruction of graft tissue, Fas/FasL interactions may have a beneficial role in transplantation. Recent studies suggest that modulation of FasL in target tissue leads to deletion, via apoptosis, of graft infiltrating lymphoid cells. However, an equally compelling series of reports indicate that overexpression of FasL can lead to a heightened immune response. These data are reviewed in the context of strategies to achieve long term allograft survival.
Fas/Fas配体（FasL）途径已被证明在T淋巴细胞介导的细胞死亡中起重要作用，并且是限制抗原激活淋巴细胞扩增的关键外周免疫调节机制。心脏、肺、肾和肝脏等常见移植器官中Fas的表达表明，这些组织可能是表达FasL的同种异体特异性细胞毒性T淋巴细胞的靶标。在这篇综述中，我们讨论了将Fas/FasL系统作为组织损伤中潜在细胞效应途径的当前文献。除了在移植组织破坏中起有害作用外，Fas/FasL相互作用在移植中可能具有有益作用。最近的研究表明，靶组织中FasL的调节可导致移植物浸润淋巴细胞通过凋亡而被清除。然而，一系列同样引人注目的报告表明，FasL的过表达可导致免疫反应增强。这些数据将在实现长期同种异体移植存活的策略背景下进行综述。
