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Correspondence response
Response to: ‘Comment on editorial ‘Pathogenic effector functions of ACPA: where do we stand’’ by Holmdahl
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  1. René Toes1,
  2. David S Pisetsky2
  1. 1 Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2 Department of Medicine, Duke University Medical Center and Medical Research Service, VA Medical Center, Durham, North Carolina, USA
  1. Correspondence to Dr René Toes, Rheumatology, Leiden University Medical Center, Leiden 31710, The Netherlands; r.e.m.toes{at}lumc.nl

https://doi.org/10.1136/annrheumdis-2019-215870

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    We have read with interest the comments by Dr Holmdahl1 on our editorial entitled ‘Pathogenic effector functions of ACPA: where do we stand?’2 and thank him for the additional information. We fully agree with him about the importance of accuracy, reliability and reproducibility of data published in the literature. Our editorial, however, was based on information available in scientific journals and focused on methodological considerations in determining the role of anti-citrullinated protein antibodies (ACPAs) in the pathogenesis of rheumatoid arthritis. We are therefore unable to comment on the issues Dr Holmdahl raises concerning the awareness of the authors of the articles in question about the problems with the monoclonal ACPAs and the timing of the correction or retraction notices.3–7 We believe that these issues can best be handled in venues in which the authors can respond and provide their own perspective.

    References

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      2. Holmdahl R
      . Comment on editorial 'Pathogenic effector functions of ACPA: where do we stand?'. Ann Rheum Dis 2020;79:e126. doi:10.1136/annrheumdis-2019-215857 pmid:http://www.ncbi.nlm.nih.gov/pubmed/31227487
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    2. ↵
      2. Toes R ,
      3. Pisetsky DS
      . Pathogenic effector functions of ACPA: Where do we stand? Ann Rheum Dis 2019;78:716–21.doi:10.1136/annrheumdis-2019-215337
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    3. ↵
      1. Anon
      . Correction: Identification of a novel chemokine-dependent molecular mechanism underlying rheumatoid arthritis-associated autoantibody-mediated bone loss. Ann Rheum Dis 2019;78:866. doi:10.1136/annrheumdis-2015-208093corr1
    4. ↵
      1. Anon
      . Correction: Autoantibodies to citrullinated proteins induce joint pain independent of inflammation via a chemokine-dependent mechanism. Ann Rheum Dis 2019;78:865. doi:10.1136/annrheumdis-2015-208094corr1
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      2. Amara K ,
      3. Steen J ,
      4. Murray F , et al
      . Retraction: Monoclonal IgG antibodies generated from joint-derived B cells of RA patients have a strong bias toward citrullinated autoantigen recognition. J Exp Med 2019;216:245. doi:10.1084/jem.2012148612112018r
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      2. Krishnamurthy A ,
      3. Joshua V ,
      4. Haj Hensvold A , et al
      . Identification of a novel chemokine-dependent molecular mechanism underlying rheumatoid arthritis-associated autoantibody-mediated bone loss. Ann Rheum Dis 2016;75:721–9.doi:10.1136/annrheumdis-2015-208093
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      2. Wigerblad G ,
      3. Bas DB ,
      4. Fernades-Cerqueira C , et al
      . Autoantibodies to citrullinated proteins induce joint pain independent of inflammation via a chemokine-dependent mechanism. Ann Rheum Dis 2016;75:730–8.doi:10.1136/annrheumdis-2015-208094
      OpenUrlAbstract/FREE Full Text

    Footnotes

    • Handling editor Josef S Smolen

    • Contributors RT and DSP wrote the response.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Provenance and peer review Commissioned; internally peer reviewed.

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