Evidence map›Paper›PMID 24337744›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Arsenic trioxide and other arsenical compounds inhibit the NLRP1, NLRP3, and NAIP5/NLRC4 inflammasomes.

Nolan K Maier, Devorah Crown, Jie Liu, Stephen H Leppla, Mahtab Moayeri

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  7. The role of TIGIT-CD226-PVR axis in mediating T cell exhaustion and apoptosis in NSCLC.Apoptosis : an international journal on programmed cell death · 2025
    Article
  8. Periodic Table of Immunomodulatory Elements and Derived Two-Dimensional Biomaterials.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  9. Article
  10. NLRP inflammasomes in health and disease.Molecular biomedicine · 2024
    Review
  11. AS3MT facilitates NLRP3 inflammasome activation by mCell biology and toxicology · 2023
    Article
  12. Systemic Lupus Erythematosus Risk: The Role of Environmental Factors.Rheumatic diseases clinics of North America · 2022
    Review
  13. Pyroptosis and pyroptosis-inducing cancer drugs.Acta pharmacologica Sinica · 2022
    Review
  14. Article
  15. Review
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  17. Review
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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

5 authors at 2 institutions in 1 country.

Nolan K MaierLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Devorah Crown
Jie Liu
Stephen H Leppla
Mahtab Moayeri
National Institute of Allergy and Infectious Diseases · USNational Heart Lung and Blood Institute · US

Funding

Vaccines and Therapeutics for AnthraxZIAAI000929 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LEPPLA, STEPHEN · 2009 to 2025
$15.9M
Intramural NIH HHS Z99 AI999999NIAID NIH HHS Y99 AI999999
6 · The paper itself

Abstract

Inflammasomes are large cytoplasmic multiprotein complexes that activate caspase-1 in response to diverse intracellular danger signals. Inflammasome components termed nucleotide-binding oligomerization domain-like receptor (NLR) proteins act as sensors for pathogen-associated molecular patterns, stress, or danger stimuli. We discovered that arsenicals, including arsenic trioxide and sodium arsenite, inhibited activation of the NLRP1, NLRP3, and NAIP5/NLRC4 inflammasomes by their respective activating signals, anthrax lethal toxin, nigericin, and flagellin. These compounds prevented the autoproteolytic activation of caspase-1 and the processing and secretion of IL-1β from macrophages. Inhibition was independent of protein synthesis induction, proteasome-mediated protein breakdown, or kinase signaling pathways. Arsenic trioxide and sodium arsenite did not directly modify or inhibit the activity of preactivated recombinant caspase-1. Rather, they induced a cellular state inhibitory to both the autoproteolytic and substrate cleavage activities of caspase-1, which was reversed by the reactive oxygen species scavenger N-acetylcysteine but not by reducing agents or NO pathway inhibitors. Arsenicals provided protection against NLRP1-dependent anthrax lethal toxin-mediated cell death and prevented NLRP3-dependent neutrophil recruitment in a monosodium urate crystal inflammatory murine peritonitis model. These findings suggest a novel role in inhibition of the innate immune response for arsenical compounds that have been used as therapeutics for a few hundred years.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigens, BacterialApoptosis Regulatory ProteinsArsenicalsArsenic TrioxideArsenitesBacterial ToxinsCalcium-Binding ProteinsCarrier ProteinsCaspase 1Cell DeathCell LineFlagellinImmunity, InnateInflammasomesAdaptor Proteins, Signal Transducinganthrax toxinAntigens, BacterialApoptosis Regulatory ProteinsArsenicalsArsenic TrioxideArsenitesBacterial ToxinsCalcium-Binding ProteinsCarrier ProteinsCaspase 1FlagellinInflammasomesInterleukin-1betaIpaf protein, mouseNaip5 protein, mouseNALP1 protein, mouseNeuronal Apoptosis-Inhibitory ProteinNigericinNitrogen OxidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseNuclear ProteinsOxidesPml protein, mousePromyelocytic Leukemia ProteinReactive Oxygen Speciessodium arseniteSodium CompoundsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID24337744
PMCPMC3884817
OpenAlexW2122125606

What OpenQuestion holds

Textmetadata
LicenceTDM
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.