ArticlePLoS pathogens2022
TLR2 axis on peripheral blood mononuclear cells regulates inflammatory responses to non-infectious immature dengue virus particles.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
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Who cites it
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 11 citations in OpenAlex.
- Mechanistic constraints in dengue severity: a systematic review with evidence stratification and agent-based evaluation of logical sufficiency.Frontiers in immunology · 2026Pooled it
- HLA alleles and dengue susceptibility across populations in the era of climate change: a comprehensive review.Frontiers in immunology · 2025Pooled it
- The contributions of TLR2, TLR8 and TLR3 to direct and antibody-dependent enhancement of dengue virus serotype 2 infection.Npj viruses · 2026Article
- Monocyte TLR2/4 as predictive biomarkers for progression from dengue warning signs to severe disease.Frontiers in immunology · 2026Article
- Early events in dengue virus infection inducing cytokine storm: The dynamic interplay of pattern-recognition receptors, inflammasome activation, and biphasic NF-κB and STAT1-dependent inflammatory responses in human mononuclear phagocytes.PLoS neglected tropical diseases · 2025Article
- Vitamin D enhances antiviral responses in dengue virus-infected macrophages by modulating early-response gene expression.PloS one · 2025Article
- E2 Ubiquitin-Conjugating Enzymes Regulates Dengue Virus-2 Replication inMicroorganisms · 2024Article
- Preliminary exploration of the role of CD14 mRNA in coronary artery injury in Kawasaki disease.American journal of translational research · 2024Article
- Scratching the Surface Takes a Toll: Immune Recognition of Viral Proteins by Surface Toll-like Receptors.Viruses · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe dengue virus (DENV) infection is characterized by exacerbated inflammatory responses that lead to endothelial dysfunction and plasma leakage. We have recently demonstrated that Toll-like receptor 2 (TLR2) on blood monocytes senses DENV infection leading to endothelial activation. Here, we report that non-infectious immature DENV particles, which are released in large numbers by DENV-infected cells, drive endothelial activation via the TLR2 axis. We show that fully immature DENV particles induce a rapid, within 6 hours post-infection, inflammatory response in PBMCs. Furthermore, pharmacological blocking of TLR2/TLR6/CD14 and/or NF-kB prior to exposure of PBMCs to immature DENV reduces the initial production of inter alia TNF-α and IL-1β by monocytes and prevents endothelial activation. However, prolonged TLR2 block induces TNF-α production and leads to exacerbated endothelial activation, indicating that TLR2-mediated responses play an important role not only in the initiation but also the resolution of inflammation. Altogether, these data indicate that the maturation status of the virus has the potential to influence the kinetics and extent of inflammatory responses during DENV infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.