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Editorial

(Auto)immunity to cartilage matrix proteins - a time bomb?

Raimund W Kinne

Author Affiliations

AG Experimentelle Rheumatologie (Experimental Rheumatology Unit), Lehrstuhl fuer Orthopaedie, Friedrich Schiller Universitaet Jena, Waldkrankenhaus 'Rudolf-Elle' GmbH, Klosterlausnitzer Straße 81, D-07607 Eisenberg, Germany

Arthritis Research & Therapy 2012, 15:101  doi:10.1186/ar4123


See related article by Geng et al., http://arthritis-research.com/content/14/4/R191

Published: 21 January 2013

Abstract

Geng and colleagues consolidate and detail the role of cartilage oligomeric matrix protein (COMP) as a (potential) autoantigen in experimental and human arthritis, a finding also supported by the detection of COMP fragments and anti-COMP antibodies in rheumatoid arthritis serum and/or synovial fluid and by synovial B-cell responses against COMP. The reactivity to COMP is yet another example of how, in addition to collagen II and the large aggregating proteoglycan, cartilage-specific proteins can induce arthritis and contribute to autoimmunity. Progression of cartilage damage and degradation in disease is believed to promote the autoimmune reaction to cartilage components. However, Geng and colleagues show that anti-COMP mAbs bind in vivo to undamaged cartilage, as previously also observed for anti-collagen II antibodies. Whether this autoimmunity also involves modifications of cartilage matrix proteins, such as citrullination, remains to be further investigated. Latent, subpathogenic (auto)immune reactions directed against cartilage matrix proteins may thus eventually contribute to the outbreak of human arthritis.