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SARS-CoV-2 antibody response after COVID-19 in patients with rheumatic disease
  1. Kristin M D’Silva1,
  2. Naomi Serling-Boyd1,
  3. Tiffany Y-T Hsu2,
  4. Jeffrey A Sparks2,
  5. Zachary S Wallace1
  1. 1 Rheumatology Unit, Massachusetts General Hospital, Boston, Massachusetts, USA
  2. 2 Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Zachary S Wallace, Rheumatology Unit, Massachusetts General Hospital, Boston, MA 02114, USA; zswallace{at}

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The impacts of rheumatic disease and immunosuppression on the development of antibodies to SARS-CoV-2 are unknown. A study of healthcare workers showed that detectable SARS-CoV-2 antibodies were associated with reduced risk of SARS-CoV-2 reinfection, and the robustness of this neutralising antibody response has implications for seroprevalence studies and vaccine efficacy.1 While disease-modifying antirheumatic drugs (DMARDs) generally blunt the immune response to pathogens, immunosuppressive medications such as dexamethasone and baricitinib have efficacy in reducing the severity of COVID-19.2 3 Additionally, tumour necrosis factor inhibition has been proposed as a potential mechanism for enhancing germinal centre formation and antibody production in severe COVID-19.4 Understanding the SARS-CoV-2 antibody response after COVID-19 among rheumatic disease patients is therefore of particular interest.5

We examined the SARS-CoV-2 antibody response among patients with rheumatic diseases and past COVID-19 at the Mass General Brigham (MGB) health system in Boston, Massachusetts, USA. Patients with COVID-19 confirmed by positive PCR testing and rheumatic disease confirmed by electronic health record (EHR) review were identified as previously described.6 …

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  • JAS and ZSW are joint senior authors.

  • Handling editor Josef S Smolen

  • Twitter @jeffsparks

  • Contributors KMD’S, NS-B, TH, JAS and ZSW contributed to the conception and drafting of the article. All listed authors provided critical revision for important intellectual content and final approval.

  • Funding KMD and NSB are supported by the National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award [T32-AR-007258]. KMD is supported by the Rheumatology Research Foundation Scientist Development Award. JAS is funded by NIH/NIAMS (grant numbers K23 AR069688, R03 AR075886, L30 AR066953, P30 AR070253, and P30 AR072577), the Rheumatology Research Foundation R Bridge Award, the Brigham Research Institute, and the R. Bruce and Joan M. Mickey Research Scholar Fund. ZSW is funded by NIH/NIAMS [K23AR073334 and L30 AR070520].

  • Competing interests JAS reports research support from Amgen and Bristol-Myers Squibb and consultancy fees from Bristol-Myers Squibb, Gilead, Inova, Janssen, Optum and Pfizer. ZSW reports research support from Bristol-Myers Squibb and Principia and consulting fees from Viela Bio and MedPace. All other authors report no competing interests.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

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