期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/ijms21114015
关键词
anti-citrullinated protein antibodies; rheumatoid arthritis; pathogenesis
资金
- Ministry of Science and Technology, Taiwan, R.O.C. [MOST 107-2314-B-182A-132-MY3]
- Chang Gung Memorial Hospital, Taiwan, R.O.C. [CMRPG3J1901-2, CMRPG3G1191, CMRPG1H0101]
Individuals with high anti-citrullinated protein antibody (ACPA) titers have an increased risk of developing rheumatoid arthritis (RA). Although our knowledge of the generation and production of ACPAs has continuously advanced during the past decade, our understanding on the pathogenic mechanisms of how ACPAs interact with immune cells to trigger articular inflammation is relatively limited. Citrullination disorders drive the generation and maintenance of ACPAs, with profound clinical significance in patients with RA. The loss of tolerance to citrullinated proteins, however, is essential for ACPAs to exert their pathogenicity. N-linked glycosylation, cross-reactivity and the structural interactions of ACPAs with their citrullinated antigens further direct their biological functions. Although questions remain in the pathogenicity of ACPAs acting as agonists for a receptor-mediated response, immune complex (IC) formation, complement system activation, crystallizable fragment gamma receptor (Fc gamma R) activation, cross-reactivity to joint cartilage and neutrophil extracellular trap (NET)-related mechanisms have all been suggested recently. This paper presents a critical review of the characteristics and possible biological effects and mechanisms of the immunopathogenesis of ACPAs in patients with RA.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据