Evidence map›Paper›PMID 25566258›Full record

ReviewFrontiers in immunology2014

Dendritic cells in dengue virus infection: targets of virus replication and mediators of immunity.

Michael A Schmid, Michael S Diamond, Eva Harris

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
11.9field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 130 citations in OpenAlex.

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  8. Glycosylation of GETV E2 promotes pathogenesis in animal models.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Innate Immune and Inflammatory Responses to Dengue Virus Infection.Current topics in microbiology and immunology · 2026
    Review
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22 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Michael A SchmidDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California Berkeley , Berkeley, CA , USA.
Michael S DiamondDepartment of Medicine, Washington University School of Medicine , St. Louis, MO , USA ; Department of Molecular Microbiology, Washington University School of Medicine , St. Louis, MO , USA ; Department of Pathology and Immunology, Washington University School of Medicine , St. Louis, MO , USA.
Eva HarrisDivision of Infectious Diseases and Vaccinology, School of Public Health, University of California Berkeley , Berkeley, CA , USA.
University of California, Berkeley · USWashington University in St. Louis · US

Funding

Safe Antibody Prophylaxis and Therapy Against Dengue VirusU01AI077955 · NIAID · WASHINGTON UNIVERSITY · PI DIAMOND, MICHAEL S · 2008 to 2011
$3.4M
Determinants of protection and enhancement of dengue infection/disease in vivoR01AI085607 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI HARRIS, EVA · 2010 to 2013
$1.5M
NIAID NIH HHS R01 AI085607NIAID NIH HHS U01 AI077955
6 · The paper itself

Abstract

Dendritic cells (DCs) are sentinels of the immune system and detect pathogens at sites of entry, such as the skin. In addition to the ability of DCs to control infections directly via their innate immune functions, DCs help to prime adaptive B- and T-cell responses by processing and presenting antigen in lymphoid tissues. Infected Aedes aegypti or Aedes albopictus mosquitoes transmit the four dengue virus (DENV) serotypes to humans while probing for small blood vessels in the skin. DENV causes the most prevalent arthropod-borne viral disease in humans, yet no vaccine or specific therapeutic is currently licensed. Although primary DENV infection confers life-long protective immunity against re-infection with the same DENV serotype, secondary infection with a different DENV serotype can lead to increased disease severity via cross-reactive T-cells or enhancing antibodies. This review summarizes recent findings in humans and animal models about DENV infection of DCs, monocytes, and macrophages. We discuss the dual role of DCs as both targets of DENV replication and mediators of innate and adaptive immunity, and summarize immune evasion strategies whereby DENV impairs the function of infected DCs. We suggest that DCs play a key role in priming DENV-specific neutralizing or potentially harmful memory B- and T-cell responses, and that future DC-directed therapies may help induce protective memory responses and reduce dengue pathogenesis.

Indexed as

antibody-dependent enhancementdendritic cellsdengue virusimmune evasioninnate immunitymacrophagesmonocytes

Identifiers

PMID25566258
PMCPMC4269190
OpenAlexW2110058049

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.