Autoantibodies to type II collagen in rheumatoid arthritis and juvenile idiopathic arthritis: meaning and clinical interest

Glaucy Rodrigues De Araújo ,Luíz Ricardo Goulart ,Carlos Ueira-Vieira

doi:10.14800/ics.813

Glaucy Rodrigues De Araújo , Luíz Ricardo Goulart + Show 1 more

Open Access

https://doi.org/10.14800/ics.813

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Abstract

Type II collagen (CII) is the major protein in articular cartilage. Autoantibodies to native and denatured CII (anti-CII) have been reported in rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). The real meaning of the anti-CII antibodies appearance is still an open question. Anti-CII antibodies may occur more commonly very early in the disease course, suggesting that these autoantibodies could be associated with the pathophysiology of RA and JIA. This finding is supported by the fact that in collagen antibody-induced arthritis (CAIA) mouse model, immunization with anti-CII antibodies directed towards several epitopes on CII in joint cartilage can induce polyarthritis that shares several pathological features with RA. This review focuses on the inflammatory events that may be associated with anti-CII production and also the clinical application of these antibodies in RA and JIA.

Highlights

In mice susceptible to experimental collagen-induced arthritis (CIA), an autoimmune polyarthritis that shares several pathological features with rheumatoid arthritis (RA) can be induced by immunization with CII
This review focuses on the inflammatory events that may be associated with anti-CII production and the clinical application of these antibodies in RA and juvenile idiopathic arthritis (JIA)
In mice susceptible to experimental collagen-induced arthritis (CIA), an autoimmune polyarthritis that shares several pathological features with RA can be induced by immunization with CII

Summary

CII degradation and cartilage damage

Articular cartilage damage is one of the key features of RA, leading to a loss of joint function [2]. A thin layer of proteinaceous material covers the cartilage surface [15] inhibiting anti-CII antibodies binding [16]. CII epitopes are exposed to antibodies due to disruption of this proteinaceous layer. High levels of anti-CII antibodies might degrade CII molecules and induce an acute inflammation mediated by surface-bound immune complexes (ICs) containing antibodies against CII [7], which leads to the complement system activation and stimulate the production of proinflammatory cytokines such as tumor necrosis factor α (TNFα), interleukin-1β (IL-1β) and IL-8 [17], contributing for perpetuation of joint inflammation and cartilage damage. Antibodies to major CII epitopes are present at the inflammation site in RA patients, and have been detected in serum and synovial fluid samples from these patients, supporting the notion of a local increased immune response to CII in the joints [18]. The involvement of anti-CII antibodies in the RA pathogenesis is still an open question, they could be useful as markers for the biomonitoring of joint destruction in some patients

CII structure

Findings

Conflict of interest