Evidence map›Paper›PMID 24995344›Full record

ArticleJournal of immunology research2014

Multiple roles of Myd88 in the immune response to the plague F1-V vaccine and in protection against an aerosol challenge of Yersinia pestis CO92 in mice.

Jennifer L Dankmeyer, Randy L Fast, Christopher K Cote, Patricia L Worsham, David Fritz, Diana Fisher, Steven J Kern, Tod Merkel, Carsten J Kirschning, Kei Amemiya

Open access · goldAbstract read
In one paragraph

Article in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 87% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Plague vaccines: new developments in an ongoing search.Applied microbiology and biotechnology · 2021
    Review
  3. 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

10 authors at 3 institutions in 2 countries.

Jennifer L DankmeyerUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
Randy L FastUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
Christopher K CoteUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
Patricia L WorshamUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
David FritzUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
Diana FisherUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
Steven J KernUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
Tod MerkelCenter of Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, MD 20892, USA.
Carsten J KirschningInstitute of Medical Microbiology, University Duisburg-Essen, Essen, Germany.
Kei AmemiyaUS Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21703, USA.
United States Army Medical Research Institute of Infectious Diseases · USCenter for Biologics Evaluation and Research · USUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current candidate vaccine against Yersinia pestis infection consists of two subunit proteins: the capsule protein or F1 protein and the low calcium response V protein or V-antigen. Little is known of the recognition of the vaccine by the host's innate immune system and how it affects the acquired immune response to the vaccine. Thus, we vaccinated Toll-like receptor (Tlr) 2, 4, and 2/4-double deficient, as well as signal adaptor protein Myd88-deficient mice. We found that Tlr4 and Myd88 appeared to be required for an optimal immune response to the F1-V vaccine but not Tlr2 when compared to wild-type mice. However, there was a difference between the requirement for Tlr4 and MyD88 in vaccinated animals. When F1-V vaccinated Tlr4 mutant (lipopolysaccharide tolerant) and Myd88-deficient mice were challenged by aerosol with Y. pestis CO92, all but one Tlr4 mutant mice survived the challenge, but no vaccinated Myd88-deficient mice survived the challenge. Spleens from these latter nonsurviving mice showed that Y. pestis was not cleared from the infected mice. Our results suggest that MyD88 appears to be important for both an optimal immune response to F1-V and in protection against a lethal challenge of Y. pestis CO92 in F1-V vaccinated mice.

Indexed as

AnimalsAntibodies, BacterialCytokinesDisease Models, AnimalFemaleMiceMice, KnockoutMyeloid Differentiation Factor 88PlaguePlague VaccineSpleenToll-Like Receptor 4Yersinia pestisAntibodies, BacterialCytokinesMyeloid Differentiation Factor 88Plague VaccineToll-Like Receptor 4

Identifiers

PMID24995344
PMCPMC4065692
OpenAlexW2157141132

What OpenQuestion holds

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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.