Evidence map›Paper›PMID 41998173›Full record

ArticleNpj viruses2026

The contributions of TLR2, TLR8 and TLR3 to direct and antibody-dependent enhancement of dengue virus serotype 2 infection.

B M Ter Ellen, M Punekar, J A Castillo, J F Valdés-López, V Upasani, S Sann, M Karnthaler, B Martija, J Moser, J M Smit and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Npj viruses, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

B M Ter EllenDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
M Punekar *Department of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
J A Castillo *Department of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
J F Valdés-LópezDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
V UpasaniDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
S SannImmunology Unit, Institut Pasteur du Cambodge, Pasteur Network, Phnom Penh, Cambodia.
M KarnthalerDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
B MartijaDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
J MoserDepartments of Critical Care, Pathology & Medical Biology, Medical Biology section, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
J M SmitDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
T CantaertImmunology Unit, Institut Pasteur du Cambodge, Pasteur Network, Phnom Penh, Cambodia.
I A Rodenhuis-ZybertDepartment of Medical Microbiology and Infection Prevention, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands. i.a.rodenhuis-zybert@umcg.nl.

Funding

NIH-PICREID 1U01AI151758
6 · The paper itself

Abstract

Antibody-dependent enhancement (ADE) of dengue virus-type 2 (DENV2) is a major risk factor for severe disease, facilitating Fcγ receptor-mediated viral entry and triggering inflammation that compromises vascular integrity. While Toll-like receptor 2 (TLR2) on monocytes promotes DENV2, strain 16681 infection in these cells and triggers an inflammatory response that activates the endothelium, its contribution to ADE remains unclear. Here, using peripheral blood mononuclear cells, we compared FcγRII (CD32)-mediated ADE infection with direct infection and assessed the contributions of TLR2, RNA sensors (TLR8, TLR3), and spleen tyrosine kinase (SYK). Blocking CD32 or SYK reduced antibody-enhanced infection to direct infection levels, whereas TLR2 inhibition abolished infection entirely. Furthermore, TLR8, TLR3, and SYK mediated inflammatory responses under both ADE and direct infection. These findings identify TLR2 as indispensable also for CD32/SYK-driven viral entry and implicate TLR8, TLR3, and SYK in ADE-associated inflammation. Our study provides mechanistic insight into ADE pathogenesis and highlights potential targets for mitigating severe dengue outcomes.

Identifiers

PMID41998173
PMCPMC13090376

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.