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The fibrillar protein collagen type II (CII) is essentially confined to hyaline cartilage in diarthrodial joints. Antibodies against CII (anti-CII) were previously described in 3%–27% of rheumatoid arthritis (RA) patients, and Kim et al described anti-CII to be associated with elevated levels of C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) in a heterogeneous group of RA patients with 2–432 months of disease duration.1 Contrary to anticitrullinated protein antibodies, anti-CII are not detected before RA onset.2 We have shown that anti-CII levels are highest at the time of RA diagnosis and thereafter decline, and that elevated anti-CII levels at diagnosis associate with elevated CRP, ESR, swollen joint count, disease activity score and radiological destruction at the time of diagnosis but not later, thus representing an acute onset RA phenotype.3–5 It is plausible that production of pro-inflammatory cytokines by macrophages …
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