Manzi S, Ahearn J M, Salmon J
Lupus Center of Excellence, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
Lupus. 2004;13(5):298-303. doi: 10.1191/0961203303lu1016oa.
Studies performed during the past several decades have demonstrated a role for the complement system in both the etiology and pathogenesis of systemic lupus erythematosus (SLE). However the specifically defective molecular and cellular pathways responsible for the disease and its complications have generally not been identified. In this report, we describe two recent advances in complement pathobiology that highlight future directions for promising investigation toward enhancing our capacity to diagnose SLE, to monitor activity of the disease, and to identify molecular and cellular defects in SLE that can be targeted by therapeutic inhibitors of complement activation. In the first example, we describe recently developed assays to detect erythrocyte C4d and complement receptor 1 for diagnosis and monitoring of disease activity in SLE. In the second example, we describe a recently discovered role for complement in mediating fetal loss in antiphospholipid syndrome and discuss the potential for this observation to facilitate identification and development of complement based biomarkers to predict poor fetal outcome in pregnant patients with SLE. These two examples are meant to underscore the importance of complement in the etiology and pathogenesis of SLE and its complications, and to stress the need for further investigation focused on the link between the complement system and SLE.
过去几十年开展的研究已证明补体系统在系统性红斑狼疮（SLE）的病因学和发病机制中发挥作用。然而，导致该疾病及其并发症的具体缺陷分子和细胞途径通常尚未明确。在本报告中，我们描述了补体病理生物学的两项最新进展，突出了未来有前景的研究方向，以提高我们诊断SLE、监测疾病活动以及识别SLE中可被补体激活治疗性抑制剂靶向的分子和细胞缺陷的能力。在第一个例子中，我们描述了最近开发的检测红细胞C4d和补体受体1的检测方法，用于诊断和监测SLE中的疾病活动。在第二个例子中，我们描述了补体在介导抗磷脂综合征胎儿丢失中的最新发现作用，并讨论了这一观察结果促进识别和开发基于补体的生物标志物以预测SLE孕妇不良胎儿结局的潜力。这两个例子旨在强调补体在SLE及其并发症的病因学和发病机制中的重要性，并强调需要进一步研究补体系统与SLE之间的联系。
