Evolution of autoantibody responses in individuals at risk of rheumatoid arthritis

被引:12
|
作者
Falkenburg, Willem J. J. [1 ,2 ]
van Schaardenburg, Dirkjan [1 ,3 ]
机构
[1] Amsterdam Rheumatol & Immunol Ctr, Reade, Doctor Jan Van Breemenstr 2, NL-1056 AB Amsterdam, Netherlands
[2] Sanquin Res, Dept Immunopathol, POB 9892, NL-1006 AN Amsterdam, Netherlands
[3] Acad Med Ctr, Amsterdam Rheumatol & Immunol Ctr, POB 22660, NL-1100 DD Amsterdam, Netherlands
来源
BEST PRACTICE & RESEARCH IN CLINICAL RHEUMATOLOGY | 2017年 / 31卷 / 01期
关键词
Arthralgia; Pre-clinical rheumatoid arthritis; Rheumatoid factors; Anti-citrullinated protein antibodies; Epitope spreading; Glycosylation; Autoantibody interactions; CITRULLINATED PROTEIN ANTIBODIES; COLLAGEN-INDUCED ARTHRITIS; CD5+ B-CELLS; CONSTANT-REGION; INTRAVENOUS IMMUNOGLOBULINS; SEROPOSITIVE ARTHRALGIA; CARBAMYLATED PROTEINS; MEDIATED INFLAMMATION; AUTOIMMUNE-DISEASES; PEPTIDE ANTIBODIES;
D O I
10.1016/j.berh.2017.07.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Autoantibodies such as rheumatoid factors (RFs), anti-citrullinated protein antibodies (ACPAs), and other anti-modified protein anti-bodies are important risk factors for the development of rheumatoid arthritis (RA) and probably play an important role in its pathogenesis. In the phase before clinical arthritis becomes apparent, different autoantibody responses can evolve because of increases in their level, isotype switching, affinity maturation, epitope spreading, and a changing glycosylation profile. This evolution may be crucial for the pathogenic properties of the autoantibody responses, and interfering with this process in individuals at risk may become a route to prevent RA. Recent data suggest that interactions between RFs and ACPAs further amplify their inflammatory potential. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:42 / 52
页数:11
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