Peripheral and synovial mechanisms of humoral autoimmunity in rheumatoid arthritis

被引:6
|
作者
Corsiero, Elisa [1 ]
Pitzalis, Costantino [1 ]
Bombardieri, Michele [1 ]
机构
[1] Queen Mary Univ London, Barts & London Sch Med & Dent, John Vane Sci Ctr, Ctr Expt Med & Rheumatol,William Harvey Res Inst, London EC1M 6BQ, England
基金
英国医学研究理事会;
关键词
B-CELL SUBPOPULATIONS; CLASS SWITCH RECOMBINATION; PLASMA-CELLS; LYMPHOID NEOGENESIS; SALIVARY-GLANDS; BLOOD; EXPRESSION; ACCUMULATION; FIBROBLASTS; EXCLUSION;
D O I
10.1016/j.drudis.2014.05.017
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
One of the hallmarks of rheumatoid arthritis (RA) is the development of humoral autoimmunity resulting in circulating autoantibodies. The clinical efficacy of B cell-depleting biologic treatments highlighted a key role for autoreactive B cell activation in the pathogenesis of RA. In this review, we discuss the key mechanisms leading to breach of B cell self-tolerance in the peripheral compartment. We also highlight the contribution of synovial ectopic lymphoid structures (ELS) in the development of functional niches of autoreactive B cells promoting humoral autoimmunity in the inflamed RA joints over and above secondary lymphoid organs (SLO).
引用
收藏
页码:1161 / 1165
页数:5
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