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SARS-CoV-2 vaccination in rituximab-treated patients: evidence for impaired humoral but inducible cellular immune response
  1. Michael Markus Bonelli1,
  2. Daniel Mrak1,
  3. Thomas Perkmann2,
  4. Helmuth Haslacher2,
  5. Daniel Aletaha1
  1. 1 Division of Rheumatology, Medical University of Vienna, Vienna, Austria
  2. 2 Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria
  1. Correspondence to Professor Daniel Aletaha, Division of Rheumatology, Medical University of Vienna, Vienna, Austria; daniel.aletaha{at}meduniwien.ac.at

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Treatment with rituximab (RTX), a monoclonal antibody targeting CD20, constitutes an important therapeutic strategy for patients with inflammatory rheumatic diseases. Some recent reports have already highlighted the risk of SARS-CoV-2 infection in patients treated with RTX.1–4 Besides the risk of a more severe disease course during B cell depleting therapy, a major concern relates to a risk of reduced immunogenicity of vaccination. Therefore, the question arises if patients should withhold or interrupt RTX therapy around COVID-19 vaccination or delay vaccination. To address this question, we have assessed antibody response and T cell mediated immune response to the BNT162b2 (Pfizer/BioNTech) vaccine in patients undergoing RTX treatment at the end of the treatment interval.

Five patients under regular and recent RTX treatment were selected for COVID-19 vaccination with BNT162b2 (Pfizer/BioNTech). A detailed description of the methods and the patient characteristics (online supplemental table S1) can be found in the online supplemental material. The last RTX infusion was administered between 4 and 12 months ago (online supplemental figure S1). At the time of the vaccination, peripheral CD19+ B cells could only be detected in two patients (online supplemental table S2). Antibodies against the SARS-CoV-2 nucleocapsid …

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Footnotes

  • Handling editor Gerd-Rüdiger R Burmester

  • Contributors All authors contributed to manuscript preparation. MMB and DA contributed to the study design. TP and HH contributed to antibody measurement.

  • Funding We do not declare a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors. However, the QuantiFERON SARS-CoV-2 RUO was kindly provided by the manufacturer (Qiagen).

  • Competing interests None declared.

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

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.