tetano
Editor, Senior Moderator
Front Immunol
. 2025 Mar 17:16:1556731.
doi: 10.3389/fimmu.2025.1556731. eCollection 2025. Non-neutralizing anti-type I interferon autoantibodies could increase thrombotic risk in critical COVID-19 patients
Mario Framil[SUP] 1 2 [/SUP], Lydia García-Serrano[SUP] 2 [/SUP], Francisco Morandeira[SUP] 2 [/SUP], Juan Francisco Luchoro[SUP] 1 [/SUP], Arnau Antolí[SUP] 3 4 [/SUP], Jose Luis Gomez-Vazquez[SUP] 3 [/SUP], Àngels Sierra-Fortuny[SUP] 3 [/SUP], Xavier Solanich[SUP] 3 4 [/SUP]
Affiliations
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.
Keywords: COVID-19; ICU patients; endothelial dysfunction; non-neutralizing autoantibodies; thrombotic complications; type I interferon.
. 2025 Mar 17:16:1556731.
doi: 10.3389/fimmu.2025.1556731. eCollection 2025. Non-neutralizing anti-type I interferon autoantibodies could increase thrombotic risk in critical COVID-19 patients
Mario Framil[SUP] 1 2 [/SUP], Lydia García-Serrano[SUP] 2 [/SUP], Francisco Morandeira[SUP] 2 [/SUP], Juan Francisco Luchoro[SUP] 1 [/SUP], Arnau Antolí[SUP] 3 4 [/SUP], Jose Luis Gomez-Vazquez[SUP] 3 [/SUP], Àngels Sierra-Fortuny[SUP] 3 [/SUP], Xavier Solanich[SUP] 3 4 [/SUP]
Affiliations
- PMID: 40165950
- PMCID: PMC11955489
- DOI: 10.3389/fimmu.2025.1556731
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.
Keywords: COVID-19; ICU patients; endothelial dysfunction; non-neutralizing autoantibodies; thrombotic complications; type I interferon.