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Patients with immune-mediated inflammatory diseases (IMID) have largely been excluded in clinical trials of SARS-CoV-2 mRNA vaccines due to both disease status and immunotherapeutics used. A recent study by Geisen et al has shown that patients with IMID using immunotherapeutics exhibited significantly lower antibody titres against the SARS-CoV-2 spike protein (S) after full vaccination with a SARS-CoV-2 mRNA vaccine relative to vaccinated healthy controls (HCs), suggesting a compromised SARS-CoV-2 mRNA vaccine antibody response in this population.1 Furthermore, a separate study by Boyarsky et al found that a proportion of patients with IMID with or without immunomodulatory therapy failed to seroconvert after the first dose with a SARS-CoV-2 mRNA vaccine.2 Here, we quantified SARS-CoV-2 mRNA vaccine-induced anti-S and receptor-binding domain (RBD) antibodies among fully vaccinated HCs and found that antibody levels in patients with IMID using immunotherapeutics were significantly lower than HCs.
A total of 66 HCs and 8 patients with IMID who had been fully vaccinated (BNT162b2 or mRNA-1273) for at least 2 weeks were recruited. All participants received their first vaccination between 13 December 2020 and 5 February 2021 and the second dose between 3 January 2021 and 5 March 2021. Individuals with known prior SARS-CoV-2 infection were excluded. IMID diagnoses included psoriasis, rheumatoid arthritis, systemic lupus erythematosus (SLE), mixed connective tissue disease, hidradenitis suppurativa and inflammatory bowel disease. All patients with IMID were on an immunomodulatory therapy, including biologic and non-biologic disease-modifying antirheumatic …
Footnotes
JV and JW contributed equally.
Contributors JV: study conception, drafting the manuscript and data analysis. KM-M:, study conception and manuscript editing. JW, TL and BZ: sample processing, data generation and analysis. IH: patient recruitment. LZ: study conception, manuscript editing and funding. Q-SM: study conception, data analysis, manuscript editing and funding.
Funding This publication presents independent research funded by the NIH/NIAMS R01AR063611 (Q-SM), Henry Ford Immunology Program T71017 (Q-SM) and T71016 (LZ).
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
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