Evidence map›Paper›PMID 21098108›Full record

ArticleInfection and immunity2011

NALP1 influences susceptibility to human congenital toxoplasmosis, proinflammatory cytokine response, and fate of Toxoplasma gondii-infected monocytic cells.

William H Witola, Ernest Mui, Aubrey Hargrave, Susan Liu, Magali Hypolite, Alexandre Montpetit, Pierre Cavailles, Cordelia Bisanz, Marie-France Cesbron-Delauw, Gilbert J Fournié and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Review
  7. International journal of molecular sciences · 2024
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  8. Article
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  10. Article
  11. Review
  12. Review
  13. Host E3 ubiquitin ligase ITCH mediatesbioRxiv : the preprint server for biology · 2023
    Article
  14. The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Variation in CD8 T cell IFNγ differentiation to strains ofFrontiers in cellular and infection microbiology · 2023
    Article
  20. Review

47 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

11 authors at 6 institutions in 3 countries.

William H WitolaDepartment of Surgery (Ophthalmology), The University of Chicago, Chicago, IL 60637, USA.
Ernest Mui
Aubrey Hargrave
Susan Liu
Magali Hypolite
Alexandre Montpetit
Pierre Cavailles
Cordelia Bisanz
Marie-France Cesbron-Delauw
Gilbert J Fournié
Rima McLeod
University of Chicago · USUniversité Joseph Fourier · FRCentre National de la Recherche Scientifique · FRMcGill University and Génome Québec Innovation Centre · CAUniversité Grenoble Alpes · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

TREATMENT OF CONGENITAL TOXOPLASMOSISR01AI027530 · NIAID · UNIVERSITY OF CHICAGO · PI MCLEOD, RIMA L · 1989 to 2010
$2.8M
Innate Immune Receptors for Toxoplasma gondiiR01AI071319 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GAZZINELLI, RICARDO TOSTES · 2006 to 2010
$2.7M
NIAID NIH HHS 2R01AI027530-18A2NIAID NIH HHS R01 AI027530NIAID NIH HHS R01 AI071319NIAID NIH HHS R01 AI071319-01
6 · The paper itself

Abstract

NALP1 is a member of the NOD-like receptor (NLR) family of proteins that form inflammasomes. Upon cellular infection or stress, inflammasomes are activated, triggering maturation of proinflammatory cytokines and downstream cellular signaling mediated through the MyD88 adaptor. Toxoplasma gondii is an obligate intracellular parasite that stimulates production of high levels of proinflammatory cytokines that are important in innate immunity. In this study, susceptibility alleles for human congenital toxoplasmosis were identified in the NALP1 gene. To investigate the role of the NALP1 inflammasome during infection with T. gondii, we genetically engineered a human monocytic cell line for NALP1 gene knockdown by RNA interference. NALP1 silencing attenuated progression of T. gondii infection, with accelerated host cell death and eventual cell disintegration. In line with this observation, upregulation of the proinflammatory cytokines interleukin-1β (IL-1β), IL-18, and IL-12 upon T. gondii infection was not observed in monocytic cells with NALP1 knockdown. These findings suggest that the NALP1 inflammasome is critical for mediating innate immune responses to T. gondii infection and pathogenesis. Although there have been recent advances in understanding the potent activity of inflammasomes in directing innate immune responses to disease, this is the first report, to our knowledge, on the crucial role of the NALP1 inflammasome in the pathogenesis of T. gondii infections in humans.

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCell DeathCell LineChildCytokinesFemaleGene Expression RegulationGenetic Predisposition to DiseaseHumansImmunity, InnateInfectious Disease Transmission, VerticalMonocytesNLR ProteinsPolymorphism, Single NucleotidePregnancyAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCytokinesNLRP1 protein, humanNLR Proteins

Identifiers

PMID21098108
PMCPMC3028851
OpenAlexW1990899125

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.