AI Article Synopsis
- * Researchers examined SARS-CoV-2 naive patients with specific genetic deficiencies and autoantibodies that affect IFN response to see if this impacted vaccine efficacy.
- * The study found that despite these deficiencies, the B cell response, including memory B cells and IgG production, remained robust and similar to healthy individuals, indicating type I IFN isn't essential for generating a strong vaccine-induced immune response against SARS-CoV-2.
Article Abstract
Inborn and acquired deficits of type I interferon (IFN) immunity predispose to life-threatening COVID-19 pneumonia. We longitudinally profiled the B cell response to mRNA vaccination in SARS-CoV-2 naive patients with inherited TLR7, IRF7, or IFNAR1 deficiency, as well as young patients with autoantibodies neutralizing type I IFNs due to autoimmune polyendocrine syndrome type-1 (APS-1) and older individuals with age-associated autoantibodies to type I IFNs. The receptor-binding domain spike protein (RBD)-specific memory B cell response in all patients was quantitatively and qualitatively similar to healthy donors. Sustained germinal center responses led to accumulation of somatic hypermutations in immunoglobulin heavy chain genes. The amplitude and duration of, and viral neutralization by, RBD-specific IgG serological response were also largely unaffected by TLR7, IRF7, or IFNAR1 deficiencies up to 7 mo after vaccination in all patients. These results suggest that induction of type I IFN is not required for efficient generation of a humoral response against SARS-CoV-2 by mRNA vaccines.
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Source |
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| http://dx.doi.org/10.1084/jem.20220258 | DOI Listing |
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9814155 | PMC |
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