{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T17:07:53Z","timestamp":1784740073916,"version":"3.55.0"},"reference-count":9,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,3,17]],"date-time":"2025-03-17T00:00:00Z","timestamp":1742169600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>During the COVID-19 pandemic, approximately 15% of patients with severe COVID-19 pneumonia were reported to have neutralizing anti-type I interferon (IFN) autoantibodies, which impaired the antiviral response and led to a poorer prognosis. However, the physiological impact of non-neutralizing autoantibodies remains unclear. In our cohort of COVID-19 patients admitted to intensive care, the presence of non-neutralizing anti-type I IFN autoantibodies increased the risk of thrombotic complications, likely via a cytokine carrier mechanism, prolonging the half-life of cytokines and dysregulating vascular endothelial function. Previous studies have associated non-neutralizing anti-type I IFN autoantibodies with an increased risk of cardiovascular complications in autoimmune diseases like systemic lupus erythematosus, but their relevance in infectious diseases remains uncertain. Stratifying anti-type I IFN autoantibodies based on their neutralizing capacity may have clinical significance not only in terms of susceptibility to infectious diseases but also in predicting cardiovascular and thrombotic events.<\/jats:p>","DOI":"10.3389\/fimmu.2025.1556731","type":"journal-article","created":{"date-parts":[[2025,3,17]],"date-time":"2025-03-17T05:26:27Z","timestamp":1742189187000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["Non-neutralizing anti-type I interferon autoantibodies could increase thrombotic risk in critical COVID-19 patients"],"prefix":"10.3389","volume":"16","author":[{"given":"Mario","family":"Framil","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lydia","family":"Garc\u00eda-Serrano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco","family":"Morandeira","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan Francisco","family":"Luchoro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arnau","family":"Antol\u00ed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose 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