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cc-by (c) Framil et al., 2025
Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/221578

Non-neutralizing anti-type I interferon autoantibodies could increase thrombotic risk in critical COVID-19 patients

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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.

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FRAMIL, Mario, et al. Non-neutralizing anti-type I interferon autoantibodies could increase thrombotic risk in critical COVID-19 patients. Frontiers in Immunology. 2025. Vol. 16. ISSN 1664-3224. [consulted: 9 of June of 2026]. Available at: https://hdl.handle.net/2445/221578

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