Evidence map›Paper›PMID 37429907›Full record

ArticleNature microbiology2023

Human FcγRIIIa activation on splenic macrophages drives dengue pathogenesis in mice.

Rachel Yamin, Kevin S Kao, Margaret R MacDonald, Tineke Cantaert, Charles M Rice, Jeffrey V Ravetch, Stylianos Bournazos

Open access · greenAbstract read
In one paragraph

Article in Nature microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.7field-weighted citation impact, top 3% of its field
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

30 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Dengue Dilemma: Navigating Cross-Reactivity and Immune Challenges.Current topics in microbiology and immunology · 2026
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. FcγRIIIa is a noncanonical costimulatory molecule for CD8 T cells.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Article
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

7 authors at 2 institutions in 2 countries.

Rachel YaminLaboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0002-3603-526X
Kevin S KaoLaboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY, USA.
Margaret R MacDonaldLaboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0001-5177-2068
Tineke CantaertImmunology Unit, Institut Pasteur du Cambodge, Institut Pasteur International Network, Phnom Penh, Cambodia.
Charles M RiceLaboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, USA.ORCID http://orcid.org/0000-0003-3087-8079
Jeffrey V Ravetch *Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY, USA. ravetch@rockefeller.edu.ORCID http://orcid.org/0000-0003-2024-9041
Stylianos Bournazos *Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY, USA. sbournazos@rockefeller.edu.ORCID http://orcid.org/0000-0001-5466-5620
Rockefeller University · USInstitut Pasteur du Cambodge · KH

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Understanding B cell memory in response to diverse virus infectionsU19AI111825 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 2014 to 2023
$26.0M
Unraveling yellow fever 17D vaccine attenuation: The role of type I interferon and innate immunityR01AI124690 · NIAID · ROCKEFELLER UNIVERSITY · PI Charles M Rice · 2016 to 2026
$8.3M
Mechanisms of antibody-dependent enhancement of SARS-CoV-2 infectionR01AI137276 · NIAID · ROCKEFELLER UNIVERSITY · PI Stylianos Bournazos · 2018 to 2026
$4.5M
NCI NIH HHS P30 CA008748NIAID NIH HHS R01 AI124690NIAID NIH HHS R01 AI137276NIAID NIH HHS U19 AI111825
6 · The paper itself

Abstract

Although dengue virus (DENV) infection typically causes asymptomatic disease, DENV-infected patients can experience severe complications. A risk factor for symptomatic disease is pre-existing anti-DENV IgG antibodies. Cellular assays suggested that these antibodies can enhance viral infection of Fcγ receptor (FcγR)-expressing myeloid cells. Recent studies, however, revealed more complex interactions between anti-DENV antibodies and specific FcγRs by demonstrating that modulation of the IgG Fc glycan correlates with disease severity. To investigate the in vivo mechanisms of antibody-mediated dengue pathogenesis, we developed a mouse model for dengue disease that recapitulates the unique complexity of human FcγRs. In in vivo mouse models of dengue disease, we discovered that the pathogenic activity of anti-DENV antibodies is exclusively mediated through engagement of FcγRIIIa on splenic macrophages, resulting in inflammatory sequelae and mortality. These findings highlight the importance of IgG-FcγRIIIa interactions in dengue, with important implications for the design of safer vaccination approaches and effective therapeutic strategies.

Indexed as

DengueDengue VirusAnimalsHumansImmunoglobulin GMacrophagesMiceReceptors, IgGImmunoglobulin GReceptors, IgG

Identifiers

PMID37429907
PMCPMC10753935
OpenAlexW4383868223

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.