Evidence map›Paper›PMID 19923225›Full record

ArticleThe Journal of biological chemistry2010

Helminth cysteine proteases inhibit TRIF-dependent activation of macrophages via degradation of TLR3.

Sheila Donnelly, Sandra M O'Neill, Colin M Stack, Mark W Robinson, Lynne Turnbull, Cynthia Whitchurch, John P Dalton

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. In vitro co-culture ofVirulence · 2025
    Article
  3. TRPV1+ neurons promote cutaneous immunity against Schistosoma mansoni.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Article
  4. Article
  5. Article
  6. Pathogens (Basel, Switzerland) · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Molecular Characterization of the Interplay betweenInternational journal of molecular sciences · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

21 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 3 institutions in 3 countries.

Sheila DonnellyInstitute for the Biotechnology of Infectious Diseases, University of Technology Sydney, Level 6, Building 4, Corner of Thomas and Harris Street, Ultimo, Sydney, New South Wales 2007, Australia.
Sandra M O'Neill
Colin M Stack
Mark W Robinson
Lynne Turnbull
Cynthia Whitchurch
John P Dalton
University of Technology Sydney · AUDublin City University · IENational University of Ireland, Maynooth · IE

Funding

VENOUS THROMBOEMBOLISM: GENES, RISK, MANAGEMENTP01HL046703 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MANN, KENNETH G · 1991 to 2011
$19.8M
NHLBI NIH HHS P01HL46703
6 · The paper itself

Abstract

Helminth pathogens prepare a Th2 type immunological environment in their hosts to ensure their longevity. They achieve this by secreting molecules that not only actively drive type 2 responses but also suppress type 1 responses. Here, we show that the major cysteine proteases secreted from the helminth pathogens Fasciola hepatica (FheCL1) and Schistosoma mansoni (SmCB1) protect mice from the lethal effects of lipopolysaccharide by preventing the release of inflammatory mediators, nitric oxide, interleukin-6, tumor necrosis factor alpha, and interleukin-12, from macrophages. The proteases specifically block the MyD88-independent TRIF-dependent signaling pathway of Toll-like receptor (TLR)4 and TLR3. Microscopical and flow cytometric studies, however, show that alteration of macrophage function by cysteine protease is not mediated by cleavage of components of the TLR4 complex on the cell surface but occurs by degradation of TLR3 within the endosome. This is the first study to describe a parasite molecule that degrades this receptor and pinpoints a novel mechanism by which helminth parasites modulate the innate immune responses of their hosts to suppress the development of Th1 responses.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsCysteine ProteasesCytokinesEndotoxinsFemaleHelminthsMacrophagesMiceMice, Inbred BALB CMyeloid Differentiation Factor 88NitritesRecombinant ProteinsTh1 CellsToll-Like Receptor 3Adaptor Proteins, Vesicular TransportCysteine ProteasesCytokinesEndotoxinsMyd88 protein, mouseMyeloid Differentiation Factor 88NitritesRecombinant ProteinsTicam1 protein, mouseTLR3 protein, mouseToll-Like Receptor 3

Identifiers

PMID19923225
PMCPMC2823461
OpenAlexW2058126260

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.