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Correspondence to ‘Bacterial citrullinated epitopes generated by Porphyromonas gingivalis infection—a missing link for ACPA production’
  1. Kevin Sheng-Kai Ma1,
  2. Cho-Han Chiang2,
  3. Yi-Wen Chen3,
  4. Li-Tzu Wang4
  1. 1Department of Life Science, National Taiwan University, Taipei, Taiwan
  2. 2Postgraduate Medical Education, Harvard Medical School, Boston, Massachusetts, USA
  3. 3Department of Dentistry, National Taiwan University Hospital, Taipei, Taiwan
  4. 4Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan
  1. Correspondence to Dr Kevin Sheng-Kai Ma, Department of Life Science, National Taiwan University, Taipei 10617, Taiwan;{at}

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With great interest, we read the work by Jenning et al, which proposed a mechanism by which Porphyromonas gingivalis (P.g.) is involved in rheumatoid arthritis (RA) progression by citrullinating and producing exogenously citrullinated human and bacterial epitopes.1 This commendable work elucidated the mechanism by which autocitrullinated prokaryotic peptidyl arginine deiminase (PPAD) mediates the inflammatory pathogenesis of RA. In particular, the authors demonstrated a correlation between anti-RA-PPAD and both anticitrullinated peptide/protein antibody (ACPA) levels and interstitial lung disease autoantigen reactivity. The study also provided evidence regarding how PPAD citrullinates the internal arginines of RA autoantigens.1 Moreover, the findings of this study suggested that the failure to clear P.g. induces bacterial citrullinated epitope-specific ACPAs, which might trigger ACPA-mediated autoimmunity.1 P.g. is the main pathogen responsible for periodontitis and has been proposed to be involved in stimulating self-reactive immune responses,2 3 which underlie the association …

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