Tarkowski A, Trollmo C, Seifert P S, Hansson G K
Department of Clinical Immunology, University of Göteborg, Sweden.
Rheumatol Int. 1992;12(5):201-5. doi: 10.1007/BF00302153.
The decay-accelerating factor (DAF) is a complement regulatory cell surface protein that protects cells from complement-mediated lysis. We analysed synovial tissue biopsies from patients with chronic arthritides for the presence of DAF using immunohistochemistry. DAF was expressed in the synovial lining cell layer both in rheumatoid arthritis (RA) and in osteoarthritis (OA). DAF was also on vascular endothelial cells of synovial tissue. A significant correlation was found between the expression of DAF and of HLA-DR in the lining layer, suggesting that DAF may be induced during a local inflammatory response. In addition, C5b-9 terminal complement complexes were found in several DAF-positive cases, suggesting that complement activation might, in itself, induce DAF expression. We propose that the occurrence of DAF may represent a physiological mechanism for local complement regulation in synovial tissue.
衰变加速因子（DAF）是一种补体调节性细胞表面蛋白，可保护细胞免受补体介导的溶解作用。我们采用免疫组织化学方法分析了慢性关节炎患者的滑膜组织活检标本中DAF的存在情况。在类风湿关节炎（RA）和骨关节炎（OA）患者的滑膜衬里细胞层中均检测到DAF的表达。DAF也存在于滑膜组织的血管内皮细胞上。在衬里层中，DAF的表达与HLA-DR的表达之间存在显著相关性，提示DAF可能在局部炎症反应过程中被诱导产生。此外，在一些DAF阳性病例中发现了C5b-9末端补体复合物，这表明补体激活本身可能诱导DAF的表达。我们认为，DAF的出现可能代表了滑膜组织中局部补体调节的一种生理机制。
