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Humoral and cell mediated immune response to SARS-CoV-2 vaccination in patients with immune-mediated diseases
Dorey A Glenn1, Yichun Hu1, Meghan E Free1
1University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Background:
Vaccination against SARS-CoV-2 induces an immune response that is protective against severe disease in healthy populations. However, humoral and cellular immune responses in individuals with immune-mediated diseases receiving immunosuppressive medications are not well understood.
Methods:
We conducted a single-center, prospective observational cohort study of pediatric and adult patients with vasculitis, glomerular disease, or other immune-mediated diseases. Antibody response assessed by viral neutralization and, in a subset, cellular immunity to SARS-CoV-2 vaccination were assessed before and at time points following initial and booster vaccination.
Results:
Between March 2021 and June 2022, 80 individuals with immune-mediated diseases and 12 healthy controls were enrolled and followed for a median of 11.97 months (IQR 7.64, 14.05). Following vaccination, the median percent angiotensin-converting enzyme 2 (ACE2) neutralization at V1 (1-3 months post vaccination) for patients in the immune-mediated disease cohort and healthy controls were 46.9% (IQR 0.65, 95.6) and 95.9% (IQR 94.6, 96.5), respectively. Of 26 individuals with anti-CD20 therapy exposure or laboratory evidence of B cell depletion at time of vaccination, only 11.9% had protective neutralization titers at V1. After adjustment for age, sex, BMI, race, vaccine type, and number of comorbidities, anti-CD20 exposure at time of initial vaccination remained significantly associated with a lower odds of ACE2 neutralization ≥30% at V1. The median T-ELISpot counts (RBD) at V1 for patients with immune-mediated diseases and healthy controls were comparable (16 [IQR 12, 37] and 16 [IQR 4.5, 23], respectively).
Conclusions:
Vaccination against SARS-CoV-2 during treatment with anti-CD20 antibody therapy was associated with impaired humoral immunity, but T cell responses were qualitatively preserved despite immunosuppressant exposure.
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