ArticleJournal of biomedical science2022
CLEC5A and TLR2 are critical in SARS-CoV-2-induced NET formation and lung inflammation.
Article in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.American journal of respiratory cell and molecular biology · 2026Article
- Neutrophil extracellular traps and severe mycoplasma pneumonia: A clinical observational study.Medicine · 2026Observational
- Single-cell Sequencing Reveals Neutrophil Extracellular Traps in Association with Endotheliopathy and Immunothrombosis in Hepatitis B Virus-related Acute-on-chronic Liver Failure.Journal of clinical and translational hepatology · 2026Article
- Review
- SARS-CoV-2 spike protein expression drives post-acute coagulopathy.Journal of virology · 2026Article
- Diagnosis of Dual c- and p-ANCA Vasculitis Following SARS-CoV-2 Infection: A Case Report.The American journal of case reports · 2026Article
- Big data analytics for CLEC5A dynamics based on single cell genomics and proteomics reveal its diverse functions in human diseases.Nanotheranostics · 2026Article
- Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Dual Role of Extracellular Vesicles as Orchestrators of Emerging and Reemerging Virus Infections.Cell biochemistry and biophysics · 2025Review
- Interferon Regulatory Factor 3 Exacerbates the Severity of COVID-19 in Mice.Critical care explorations · 2025Article
- Neutrophil-ACS infectious diseases · 2025Article
- TLR2 Activation as a Marker of Severe COVID-19 and a Potential Therapeutic Target.Current medicinal chemistry · 2025Review
- Sars-Cov-2 spike protein and plasma from COVID-19 patients induce extracellular traps by myeloid-derived suppressor cells.Frontiers in cellular and infection microbiology · 2025Article
- The deficient CLEC5A ameliorates the behavioral and pathological deficits via the microglial Aβ clearance in Alzheimer's disease mouse model.Journal of neuroinflammation · 2024Article
- Special Issue "The Role of Toll-Like Receptors (TLRs) in Infection and Inflammation 2.0".International journal of molecular sciences · 2024Article
- Extracellular histones: a unifying mechanism driving platelet-dependent extracellular vesicle release and thrombus formation in COVID-19.Journal of thrombosis and haemostasis : JTH · 2024Article
- Innate Immunity in Protection and Pathogenesis During Coronavirus Infections and COVID-19.Annual review of immunology · 2024Review
- Enhancement of NETosis by ACE2-cross-reactive anti-SARS-CoV-2 RBD antibodies in patients with COVID-19.Journal of biomedical science · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundCoronavirus-induced disease 19 (COVID-19) infects more than three hundred and sixty million patients worldwide, and people with severe symptoms frequently die of acute respiratory distress syndrome (ARDS). Recent studies indicated that excessive neutrophil extracellular traps (NETs) contributed to immunothrombosis, thereby leading to extensive intravascular coagulopathy and multiple organ dysfunction. Thus, understanding the mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced NET formation would be helpful to reduce thrombosis and prevent ARDS in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
methodsWe incubated SARS-CoV-2 with neutrophils in the presence or absence of platelets to observe NET formation. We further isolated extracellular vesicles from COVID-19 patients' sera (COVID-19-EVs) to examine their ability to induce NET formation.
resultsWe demonstrated that antagonistic mAbs against anti-CLEC5A mAb and anti-TLR2 mAb can inhibit COVID-19-EVs-induced NET formation, and generated clec5a
conclusionsThis study demonstrates that SARS-CoV-2-activated platelets produce EVs to enhance thromboinflammation via CLEC5A and TLR2, and highlight the importance of CLEC5A and TLR2 as therapeutic targets to reduce the risk of ARDS in COVID-19 patients.
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Registered trials
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