ArticleJournal of clinical immunology2024
Suppression of Type I Interferon Signaling in Myeloid Cells by Autoantibodies in Severe COVID-19 Patients.
Article in Journal of clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Systematic Review and Meta-analysis of Anti-interferon Auto-antibodies in Infectious Diseases.Journal of clinical immunology · 2026Pooled it
- Autoantibodies neutralizing type I interferons in COVID-19 patients from southern Brazil.Journal of human immunity · 2026Article
- Anti-Type I Interferon Autoantibodies in COVID-19 and Systemic Lupus Erythematosus: A Comparative Review.Antibodies (Basel, Switzerland) · 2026Review
- RNA and ChIP-sequencing analysis reveals SOX3 suppresses antiviral innate immunity through the AKT1-PTEN signaling axis.Virologica Sinica · 2025Article
- Distinctive Temporal Profiles of Interferon-Stimulated Genes in Natural Infection, Viral Challenge, and Vaccination.Viruses · 2025Article
- Type I interferon autoantibody footprints reveal neutralizing mechanisms and allow inhibitory decoy design.The Journal of experimental medicine · 2025Article
- Modulation of antigen delivery and lymph node activation in nonhuman primates by saponin adjuvant saponin/monophosphoryl lipid A nanoparticle.PNAS nexus · 2024Article
Corrections and comments
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Authors and funding
36 authors at 11 institutions in 1 country.
Funding
Abstract
purposeAuto-antibodies (auto-abs) to type I interferons (IFNs) have been identified in patients with life-threatening coronavirus disease 2019 (COVID-19), suggesting that the presence of auto-abs may be a risk factor for disease severity. We therefore investigated the mechanism underlying COVID-19 exacerbation induced by auto-abs to type I IFNs.
methodsWe evaluated plasma from 123 patients with COVID-19 to measure auto-abs to type I IFNs. We performed single-cell RNA sequencing (scRNA-seq) of peripheral blood mononuclear cells from the patients with auto-abs and conducted epitope mapping of the auto-abs.
resultsThree of 19 severe and 4 of 42 critical COVID-19 patients had neutralizing auto-abs to type I IFNs. Patients with auto-abs to type I IFNs showed no characteristic clinical features. scRNA-seq from 38 patients with COVID-19 revealed that IFN signaling in conventional dendritic cells and canonical monocytes was attenuated, and SARS-CoV-2-specific BCR repertoires were decreased in patients with auto-abs. Furthermore, auto-abs to IFN-α2 from COVID-19 patients with auto-abs recognized characteristic epitopes of IFN-α2, which binds to the receptor.
conclusionAuto-abs to type I IFN found in COVID-19 patients inhibited IFN signaling in dendritic cells and monocytes by blocking the binding of type I IFN to its receptor. The failure to properly induce production of an antibody to SARS-CoV-2 may be a causative factor of COVID-19 severity.
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