类风湿性关节炎
医学
自身抗体
免疫学
自身免疫
关节炎
炎症
发病机制
痹症科
瓜氨酸化
自身免疫性疾病
抗体
内科学
生物
瓜氨酸
氨基酸
精氨酸
生物化学
作者
Isao Matsumoto,Izumi Kurata,Ayako Ohyama,Hoshimi Kawaguchi,Hiroshi Ebe,Atsumu Osada,Yuya Kondo,Hiroto Tsuboi,Takayuki Sumida
标识
DOI:10.1080/14397595.2019.1659539
摘要
Rheumatoid arthritis (RA) is an inflammatory disorder characterized by synovial inflammation in multiple joints. Autoantibodies (Abs) are the hallmark of RA, and as disease-specific and diagnostic markers, rheumatoid factor and anti-citrullinated protein antibody (ACPA) are produced pre-clinically, but their pathogenic roles in RA remain elusive. In this review, we focus on one of the candidate autoantigens in RA; glucose-6-phosphate isomerase (GPI). The arthritogenic role of GPI has been confirmed in two different mouse models: the K/BxN- and GPI-induced arthritis models. Both anti-GPI Abs and citrullinated-GPI peptide Abs have been detected in human RA. Studies conducted in these rodent models have confirmed that the pathogenesis of arthritis involves the localization of autoantigens not only in the joints but also in the circulation. In this review, we revisit and summarize the arthritogenic relevance of GPI in animal RA models and in human RA, and extend the discussion to joint-specific inflammation.
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