ArticleOncotarget2017
TLR2/MyD88 pathway-dependent regulation of dendritic cells by dengue virus promotes antibody-dependent enhancement via Th2-biased immunity.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Nanoparticle vaccine formulations for dengue virus.RSC pharmaceutics · 2026Review
- Immunoinformatics and molecular modeling approaches to design a multi-epitope vaccine against Tibrovirus Congo.Open medicine (Warsaw, Poland) · 2026Article
- Optimizing the dengue virus infection mouse model: Comparing different backgrounds and infection route for enhanced stability.Animal models and experimental medicine · 2026Article
- Interplay between innate immune cells and inflammatory mediators in dengue infection: an evolving therapeutic paradigm.Expert reviews in molecular medicine · 2025Review
- Immunomodulation in dengue: towards deciphering dengue severity markers.Cell communication and signaling : CCS · 2024Review
- Article
- Zika virus-like particle vaccine fusion loop mutation increases production yield but fails to protect AG129 mice against Zika virus challenge.PLoS neglected tropical diseases · 2022Article
- Review
- Recent Insights Into the Molecular Mechanism of Toll-Like Receptor Response to Dengue Virus Infection.Frontiers in microbiology · 2021Review
- The Protective HIV-1 Envelope gp41 Antigen P1 Acts as a Mucosal Adjuvant Stimulating the Innate Immunity.Frontiers in immunology · 2020Article
- Effect of high doses of vitamin D supplementation on dengue virus replication, Toll-like receptor expression, and cytokine profiles on dendritic cells.Molecular and cellular biochemistry · 2020Article
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Possible risk mediators in primary dengue virus (DenV) infection that favor secondary DenV infection to life-threatening dengue hemorrhagic fever (DHF) and shock syndrome (DSS) via antibody-dependent enhancement (ADE) have not yet been described. Here, DenV infection enhanced the expression of inflammatory mediators and activation molecules in dendritic cells (DCs) through TLR2/MyD88 pathway. TLR2 appeared to facilitate DenV infection in DCs that were less permissive than macrophages for viral replication. In experiments using separate evaluations of DenV-infected and uninfected bystander DCs, infected DCs showed impaired maturation accompanied with TLR2-dependent production of inflammatory cytokines, by which uninfected bystander DCs showed increased expression of co-stimulatory molecules. Differential phosphorylation of MAPK and STAT3 was also detected between DenV-infected and uninfected DCs. Furthermore, DenV infection stimulated Th2-polarized humoral and cellular immunity against foreign and DenV Ag via TLR2/MyD88 pathway, and DenV-infected DCs were revealed to facilitate Th2-biased immune responses in TLR2-dependent manner. TLR2/MyD88-mediated Th2-biased Ab responses to primary DenV infection increased the infectivity of secondary homotypic or heterotypic DenV via ADE. Collectively, these results indicate that TLR2/MyD88 pathway in DC-priming receptors can drive Th2-biased immune responses during primary DenV infection, which could favor secondary DenV infection to DHF/DSS via ADE.
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