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Antibodies against collagen type II are not a general marker of acute arthritis onset
  1. Vivek Anand Manivel1,
  2. Diane van der Woude2,
  3. Rene Toes2,
  4. Andrew Filer3,4,
  5. Karim Raza3,5,
  6. Johan Rönnelid1
  1. 1 Department of Immunology Genetics and Pathology, Uppsala University, Uppsala, Sweden
  2. 2 Department of Rheumatology, Leiden University Medical Center, Leiden, Netherlands
  3. 3 Rheumatology Research Group, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
  4. 4 Department of Rheumatology, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
  5. 5 Department of Rheumatology, Sandwell and West Birmingham Hospitals NHS Trust, Birmingham, UK
  1. Correspondence to Dr Johan Rönnelid, Department Immunology, Genetics and Pathology, Uppsala University, Rudbeck Laboratory C5, Uppsala SE-75185, Sweden; johan.ronnelid{at}

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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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  • Contributors VAM and JR designed the study. DvdW, RT, AF and KR contributed with patient samples and clinical information. VAM performed anti-CII ELISA analyses, and JR drafted the text. All authors have read and contributed to the final text and also approved the submitted version.

  • Competing interests None declared.

  • Ethics approval Leiden University Medical Center and Birmingham University, respectively.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement All available data are included in the manuscript.