Autoantibodies Neutralizing Type I IFNs in the Bronchoalveolar Lavage of at Least 10% of Patients During Life-Threatening COVID-19 Pneumonia.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Philippot Quentin, Fekkar Arnaud, Gervais Adrian, Le Voyer Tom, Boers Leonoor S, Conil Clément, Bizien Lucy, de Brabander Justin, Duitman Jan Willem, Romano Alessia, Rosain Jérémie, Blaize Marion, Migaud Mélanie, Jeljeli Maxime, Hammadi Boualem, Desmons Aurore, Marchal Astrid, ArtDECO consortium, COVID HGE consortium, Mayaux Julien, Zhang Qian, Jouanguy Emmanuelle, Borie Raphael, Crestani Bruno, Luyt Charles Edouard, Adle-Biassette Homa, Sene Damien, Megarbane Bruno, Cobat Aurélie, Bastard Paul, Bos Lieuwe D J, Casanova Jean-Laurent, Puel Anne
Аннотация
Autoantibodies (auto-Abs) neutralizing type I interferons (IFNs) are found in the blood of at least 15% of unvaccinated patients with life-threatening COVID-19 pneumonia. We report here the presence of auto-Abs neutralizing type I IFNs in the bronchoalveolar lavage (BAL) of 54 of the 415 unvaccinated patients (13%) with life-threatening COVID-19 pneumonia tested. The 54 individuals with neutralizing auto-Abs in the BAL included 45 (11%) with auto-Abs against IFN-α2, 37 (9%) with auto-Abs against IFN-ω, 54 (13%) with auto-Abs against IFN-α2 and/or ω, and five (1%) with auto-Abs against IFN-β, including three (0.7%) with auto-Abs neutralizing IFN-α2, IFN-ω, and IFN-β, and two (0.5%) with auto-Abs neutralizing IFN-α2 and IFN-β. Auto-Abs against IFN-α2 also neutralize the other 12 subtypes of IFN-α. Paired plasma samples were available for 95 patients. All seven patients with paired samples who had detectable auto-Abs in BAL also had detectable auto-Abs in plasma, and one patient had auto-Abs detectable only in blood. Auto-Abs neutralizing type I IFNs are, therefore, present in the alveolar space of at least 10% of patients with life-threatening COVID-19 pneumonia. These findings suggest that these auto-Abs impair type I IFN immunity in the lower respiratory tract, thereby contributing to hypoxemic COVID-19 pneumonia.