Umeda Naoto, Matsumoto Isao, Sumida Takayuki
Department of Rheumatology, Tsuchiura Kyodo General Hospital.
Department of Internal Medicine, Faculty of Medicine, University of Tsukuba.
Nihon Rinsho Meneki Gakkai Kaishi. 2017;40(6):391-395. doi: 10.2177/jsci.40.391.
In rheumatoid arthritis (RA), ACPA (anti-citrullinated protein/peptide antibody) is elevated with high specificity, and clinically, anti-CCP (cyclic citrullinated peptide) antibody is widely used for diagnosis of RA. It is thought ACPAs are produced with genetic background such as HLA-DR, environmental factors such as periodontal disease and smoking, however, the pathogenic role of ACPA in RA has not been elucidated. These were showed immune complexes including ACPA or ACPA itself promoted inflammatory cytokine production such as TNF. PADs (peptidylarginine deiminases) were expressed and citrullinated proteins existed in RA synovium. ACPAs were deposited on the site of citrulline in CD68 positive cells of RA synovium. The damage of bone and cartilage is observed in RA. It was also suggested that deposition of ACPAs caused osteoclastogenesis and bone loss. We introduce several findings about the pathogenic role of ACPA in RA.
在类风湿关节炎(RA)中,抗瓜氨酸化蛋白/肽抗体(ACPA)特异性升高,临床上,抗环瓜氨酸肽(CCP)抗体被广泛用于RA的诊断。人们认为,ACPA是在诸如HLA - DR等遗传背景以及诸如牙周病和吸烟等环境因素作用下产生的,然而,ACPA在RA中的致病作用尚未阐明。研究表明,包括ACPA或ACPA本身的免疫复合物可促进炎性细胞因子如肿瘤坏死因子(TNF)的产生。肽基精氨酸脱氨酶(PADs)在RA滑膜中表达,且存在瓜氨酸化蛋白。ACPA沉积于RA滑膜CD68阳性细胞中的瓜氨酸位点。在RA中可观察到骨和软骨的损伤。也有研究提示,ACPA的沉积会导致破骨细胞生成和骨质流失。我们介绍一些关于ACPA在RA中致病作用的研究发现。