Evidence map›Paper›PMID 24130499›Full record

ArticlePLoS pathogens2013

Regulation of innate responses during pre-patent schistosome infection provides an immune environment permissive for parasite development.

Diana K Riner, Christine E Ferragine, Sean K Maynard, Stephen J Davies

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. TRP channels as potential targets for antischistosomals.International journal for parasitology. Drugs and drug resistance · 2018
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. TRP channels in schistosomes.International journal for parasitology. Drugs and drug resistance · 2016
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Diana K RinerDepartment of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland, United States of America.
Christine E Ferragine
Sean K Maynard
Stephen J Davies
Uniformed Services University of the Health Sciences · US

Funding

Modulation of schistosome development by T cell signalsR01AI066227 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI DAVIES, STEPHEN J · 2006 to 2009
$1.5M
NIAID NIH HHS HHSN272201000005CNIAID NIH HHS HHSN272201000005INIAID NIH HHS R01 AI066227
6 · The paper itself

Abstract

Blood flukes of the genus Schistosoma infect over 200 million people, causing granulomatous pathology with accompanying morbidity and mortality. As a consequence of extensive host-parasite co-evolution, schistosomes exhibit a complex relationship with their hosts, in which immunological factors are intimately linked with parasite development. Schistosomes fail to develop normally in immunodeficient mice, an outcome specifically dependent on the absence of CD4⁺ T cells. The role of CD4⁺ T cells in parasite development is indirect and mediated by interaction with innate cells, as repeated toll-like receptor 4 stimulation is sufficient to restore parasite development in immunodeficient mice in the absence of CD4⁺ T cells. Here we show that repeated stimulation of innate immunity by an endogenous danger signal can also restore parasite development and that both these stimuli, when administered repeatedly, lead to the regulation of innate responses. Supporting a role for regulation of innate responses in parasite development, we show that regulation of inflammation by neutralizing anti-TNF antibodies also restores parasite development in immunodeficient mice. Finally, we show that administration of IL-4 to immunodeficient mice to regulate inflammation by induction of type 2 responses also restores parasite development. These findings suggest that the type 2 response driven by CD4⁺ T cells during pre-patent infection of immunocompetent hosts is exploited by schistosomes to complete their development to reproductively mature adult parasites.

Indexed as

Immunity, InnateAnimalsAntibodies, NeutralizingHumansInterleukin-4MiceMice, KnockoutSchistosomaSchistosomiasisTh2 CellsToll-Like Receptor 4Tumor Necrosis Factor-alphaAntibodies, NeutralizingInterleukin-4Tlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID24130499
PMCPMC3795041
OpenAlexW2093734748

What OpenQuestion holds

Textmetadata
LicenceCC0
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.