ArticleNature communications2022
Circulating multimeric immune complexes contribute to immunopathology in COVID-19.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Engineering Protein-Based HIV Entry Inhibitors: Advances, Challenges, and Translational Strategies.Biomolecules · 2026Review
- Fcγ-receptor-activation by circulating immune complexes in systemic autoimmune diseases and its reduction by CD19-CAR T cell therapy.Rheumatology (Oxford, England) · 2026Article
- Article
- CoupleVAE: coupled variational autoencoders for predicting perturbational single-cell RNA sequencing data.Briefings in bioinformatics · 2025Article
- Virus-Induced Pathogenic Antibodies: Lessons from Long COVID and Dengue Hemorrhage Fever.International journal of molecular sciences · 2025Review
- Gut microbial metabolites as a convergence point between autoimmunity and solid tumors.Gut microbes reports · 2025Review
- Human Fcγ-receptors selectively respond to C-reactive protein isoforms.Frontiers in immunology · 2025Article
- FcγRIIIA -activating antibodies in dengue virus infection reveals a distinct transient cross-reactive profile.Frontiers in immunology · 2025Article
- Impaired mucosal IgA response in patients with severe COVID-19.Emerging microbes & infections · 2024Article
- Fcγ-receptor-IIIA bioactivity of circulating and synovial immune complexes in rheumatoid arthritis.RMD open · 2024Article
- Unraveling the enigma of long COVID: novel aspects in pathogenesis, diagnosis, and treatment protocols.Inflammopharmacology · 2024Review
- Article
- Structural properties of immune complexes formed by viral antigens and specific antibodies shape the inflammatory response of macrophages.Cell & bioscience · 2024Article
- Enhancement of NETosis by ACE2-cross-reactive anti-SARS-CoV-2 RBD antibodies in patients with COVID-19.Journal of biomedical science · 2024Article
- Clinical characteristics and influencing factors of severe fever with thrombocytopenia syndrome complicated by viral myocarditis: a retrospective study.BMC infectious diseases · 2024Article
- Identification of new drugs to counteract anti-spike IgG-induced hyperinflammation in severe COVID-19.Life science alliance · 2023Article
- Preliminary Comparison of Molecular Antioxidant and Inflammatory Mechanisms Determined in the Peripheral Blood Granulocytes of COVID-19 Patients.International journal of molecular sciences · 2023Article
- SARS-CoV-2 and Its Bacterial Co- or Super-Infections Synergize to Trigger COVID-19 Autoimmune Cardiopathies.International journal of molecular sciences · 2023Article
- Immune complexes as culprits of immunopathology in severe COVID-19.Medical microbiology and immunology · 2023Review
- The Low Expression of Fc-Gamma Receptor III (CD16) and High Expression of Fc-Gamma Receptor I (CD64) on Neutrophil Granulocytes Mark Severe COVID-19 Pneumonia.Diagnostics (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A dysregulated immune response with high levels of SARS-CoV-2 specific IgG antibodies characterizes patients with severe or critical COVID-19. Although a robust IgG response is considered to be protective, excessive triggering of activating Fc-gamma-receptors (FcγRs) could be detrimental and cause immunopathology. Here, we document excessive FcγRIIIA/CD16A activation in patients developing severe or critical COVID-19 but not in those with mild disease. We identify two independent ligands mediating extreme FcγRIIIA/CD16A activation. Soluble circulating IgG immune complexes (sICs) are detected in about 80% of patients with severe and critical COVID-19 at levels comparable to active systemic lupus erythematosus (SLE) disease. FcγRIIIA/CD16A activation is further enhanced by afucosylation of SARS-CoV-2 specific IgG. Utilizing cell-based reporter systems we provide evidence that sICs can be formed prior to a specific humoral response against SARS-CoV-2. Our data suggest a cycle of immunopathology driven by an early formation of sICs in predisposed patients. These findings suggest a reason for the seemingly paradoxical findings of high antiviral IgG responses and systemic immune dysregulation in severe COVID-19. The involvement of circulating sICs in the promotion of immunopathology in predisposed patients opens new possibilities for intervention strategies to mitigate critical COVID-19 progression.
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