Evidence map›Paper›PMID 19917714›Full record

ArticleInfection and immunity2010

Major secretory antigens of the helminth Fasciola hepatica activate a suppressive dendritic cell phenotype that attenuates Th17 cells but fails to activate Th2 immune responses.

David J Dowling, Clare M Hamilton, Sheila Donnelly, James La Course, Peter M Brophy, John Dalton, Sandra M O'Neill

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

72 citing papers in PubMed, 125 citations in OpenAlex.

  1. Trial
  2. Article
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  6. Article
  7. Design and Expression ofInternational journal of molecular sciences · 2025
    Article
  8. Article
  9. Article
  10. Microbiology spectrum · 2024
    Article
  11. An Update on the Pathogenesis of Fascioliasis: What Do We Know?Research and reports in tropical medicine · 2024
    Review
  12. Review
  13. Article
  14. Review
  15. Secondary infection ofFrontiers in veterinary science · 2023
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Antigen-specific response of CD4Veterinary research · 2021
    Article

12 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

7 authors at 5 institutions in 3 countries.

David J DowlingParasite Immune Modulation Group, School of Nursing, Faculty of Science and Health, Dublin City University, Glasnevin, Dublin 9, Ireland.
Clare M Hamilton
Sheila Donnelly
James La Course
Peter M Brophy
John Dalton
Sandra M O'Neill
Dublin City University · IEAberystwyth University · GBMcGill University · CANational University of Ireland, Maynooth · IEUniversity of Liverpool · GB

Funding

Biotechnology and Biological Sciences Research Council BB/C503638/1Biotechnology and Biological Sciences Research Council BB/C503638/2Biotechnology and Biological Sciences Research Council BB/H009256/1
6 · The paper itself

Abstract

Fasciola hepatica is a helminth pathogen that drives Th2/Treg immune responses in its mammalian host. The parasite releases a large number of molecules that are critical to inducing this type of immune response. Here we have selected recombinant forms of two major F. hepatica secreted molecules, the protease cathepsin L (rFhCL1) and an antioxidant, sigma class glutathione transferase (rFhGST-si), to examine their interactions with dendritic cells (DCs). Despite enzymatic and functional differences between these molecules, both induced interleukin-6 (IL-6), IL-12p40, and macrophage inflammatory protein 2 (MIP-2) secretion from DCs and enhanced CD40 expression. While this induction was mediated by Toll-like receptor 4 (TLR4), the subsequent intracellular signaling pathways differed; rFhCL1 signaled through p38, and rFhGST-si mediated its effect via c-Jun N-terminal kinase (JNK), p38, p-NF-kappaBp65, and IRF5. Neither rFhCL1 nor rFhGST-si enhanced DC phagocytosis or induced Th2 immune responses in vivo. However, DCs matured in the presence of either enzyme attenuated IL-17 production from OVA peptide-specific T cells in vivo. In addition, DCs exposed to either antigen secreted reduced levels of IL-23. Therefore, both F. hepatica FhCL1 and FhGST-si modulate host immunity by suppressing responses associated with chronic inflammation-an immune modulatory mechanism that may benefit the parasite's survival within the host.

Indexed as

AnimalsAntigens, HelminthBlotting, WesternDendritic CellsFasciola hepaticaFascioliasisInterleukin-17MiceMice, Inbred BALB CMice, Inbred C57BLPhenotypeSignal TransductionTh1 CellsTh2 CellsT-Lymphocyte SubsetsAntigens, HelminthInterleukin-17

Identifiers

PMID19917714
PMCPMC2812196
OpenAlexW2115787145

What OpenQuestion holds

Textmetadata
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.