{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T05:48:20Z","timestamp":1791870500734,"version":"4.3.4"},"reference-count":75,"publisher":"Rockefeller University Press","issue":"1","license":[{"start":{"date-parts":[[2022,11,7]],"date-time":"2022-11-07T00:00:00Z","timestamp":1667779200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,1,2]]},"abstract":"<jats:p>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)\u2013specific 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.<\/jats:p>","DOI":"10.1084\/jem.20220258","type":"journal-article","created":{"date-parts":[[2022,10,6]],"date-time":"2022-10-06T02:21:03Z","timestamp":1665022863000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":51,"title":["Human type I IFN deficiency does not impair B cell response to SARS-CoV-2 mRNA vaccination"],"prefix":"10.1084","volume":"220","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1198-8689","authenticated-orcid":true,"given":"Aur\u00e9lien","family":"Sokal","sequence":"first","affiliation":[{"name":"Necker Enfants Malades Institute, INSERM U1151\/CNRS UMR 8253, Action th\u00e9matique incitative sur programme-Avenir Team Auto-Immune and Immune B cell, University Paris Cit\u00e9, University Paris-Est-Cr\u00e9teil, Cr\u00e9teil, France 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5926-8437","authenticated-orcid":true,"given":"Paul","family":"Bastard","sequence":"additional","affiliation":[{"name":"Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France 2"},{"name":"Imagine Institute, University Paris Cit\u00e9, Paris, France 3"},{"name":"Department of Pediatrics, Necker Hospital for Sick Children, Assistance Publique-H\u00f4pitaux de Paris, Paris, France 4"},{"name":"St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 5"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9799-4608","authenticated-orcid":true,"given":"Pascal","family":"Chappert","sequence":"additional","affiliation":[{"name":"Necker Enfants Malades Institute, INSERM U1151\/CNRS UMR 8253, Action th\u00e9matique incitative sur programme-Avenir Team Auto-Immune and Immune B cell, University Paris Cit\u00e9, University Paris-Est-Cr\u00e9teil, Cr\u00e9teil, France 1"},{"name":"INSERM U955, team 2. 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