Evidence map›Paper›PMID 18802464›Full record

ArticlePLoS pathogens2008

Protective effect of Toll-like receptor 4 in pulmonary vaccinia infection.

Martha A Hutchens, Kathryn E Luker, Joanne Sonstein, Gabriel Núñez, Jeffrey L Curtis, Gary D Luker

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. TLR4 signalling: the key to controlling EV71 replication and inflammatory response.Frontiers in cellular and infection microbiology · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Toll-like Receptor Mediation in SARS-CoV-2: A Therapeutic Approach.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Innate Sensing of DNA Virus Genomes.Annual review of virology · 2018
    Review
  18. Article
  19. Article
  20. NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

6 authors at 2 institutions in 1 country.

Martha A HutchensGraduate Program in Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.
Kathryn E Luker
Joanne Sonstein
Gabriel Núñez
Jeffrey L Curtis
Gary D Luker
Michigan United · USUniversity of Michigan–Ann Arbor · US

Funding

Michigan Small Animal Imaging Resource (MSAIR)R24CA083099 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROSS, BRIAN D. · 1999 to 2006
$4.2M
Innate and adaptive immunity in COPD exacerbationsR01HL082480 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CURTIS, JEFFREY LOUIS · 2005 to 2009
$2.4M
Imaging Vaccina Viral-Host PathogenesisR21AI066192 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKER, GARY D · 2006 to 2007
$399k
NCI NIH HHS R24 CA083099NCI NIH HHS R24CA083099NHLBI NIH HHS R01 HL082480NIAID NIH HHS R21 AI066192NIAID NIH HHS R21AI066192
6 · The paper itself

Abstract

Innate immune responses are essential for controlling poxvirus infection. The threat of a bioterrorist attack using Variola major, the smallpox virus, or zoonotic transmission of other poxviruses has renewed interest in understanding interactions between these viruses and their hosts. We recently determined that TLR3 regulates a detrimental innate immune response that enhances replication, morbidity, and mortality in mice in response to vaccinia virus, a model pathogen for studies of poxviruses. To further investigate Toll-like receptor signaling in vaccinia infection, we first focused on TRIF, the only known adapter protein for TLR3. Unexpectedly, bioluminescence imaging showed that mice lacking TRIF are more susceptible to vaccinia infection than wild-type mice. We then focused on TLR4, the other Toll-like receptor that signals through TRIF. Following respiratory infection with vaccinia, mice lacking TLR4 signaling had greater viral replication, hypothermia, and mortality than control animals. The mechanism of TLR4-mediated protection was not due to increased release of proinflammatory cytokines or changes in total numbers of immune cells recruited to the lung. Challenge of primary bone marrow macrophages isolated from TLR4 mutant and control mice suggested that TLR4 recognizes a viral ligand rather than an endogenous ligand. These data establish that TLR4 mediates a protective innate immune response against vaccinia virus, which informs development of new vaccines and therapeutic agents targeted against poxviruses.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsCells, CulturedImmunity, InnateLung DiseasesMacrophagesMiceMice, KnockoutToll-Like Receptor 4VacciniaVaccinia virusAdaptor Proteins, Vesicular TransportTicam1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID18802464
PMCPMC2529451
OpenAlexW2036704208

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.