ArticleCell host & microbe2007
Microbial pathogen-induced necrotic cell death mediated by the inflammasome components CIAS1/cryopyrin/NLRP3 and ASC.
Article in Cell host & microbe, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.
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.
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.
Who cites it
154 citing papers in PubMed, 286 citations in OpenAlex.
- A pilot study to evaluate the safety and efficacy of the long-acting interleukin-1 inhibitor rilonacept (interleukin-1 Trap) in patients with familial cold autoinflammatory syndrome.Arthritis and rheumatism · 2008Trial
- Hydroxytyrosol Restrains NLRP3 Inflammasome Activation and Pyroptosis Through the TLR4/NF-κB Pathway to Prevent Mycoplasma gallisepticum-Inflammation.Poultry science · 2026Article
- Dual NLRC4 and non-canonical inflammasome signaling drives human GSDMD-mediated killing ofbioRxiv : the preprint server for biology · 2026Article
- Review
- Cannabis use is associated with alterations in NLRP3 inflammasome related gene expression in monocyte-derived macrophages from people living with HIV.Frontiers in immunology · 2025Article
- Role of NLRP3 in Parkinson's disease: Specific activation especially in dopaminergic neurons.Heliyon · 2024Review
- Mitochondrial P-JNK target, SAB (SH3BP5), in regulation of cell death.Frontiers in cell and developmental biology · 2024Review
- Cathepsin B in programmed cell death machinery: mechanisms of execution and regulatory pathways.Cell death & disease · 2023Review
- Integrative analysis highlights molecular and immune responses of tickFrontiers in cellular and infection microbiology · 2023Article
- Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022Review
- Article
- Molecular mechanisms of Shigella effector proteins: a common pathogen among diarrheic pediatric population.Molecular and cellular pediatrics · 2022Review
- Apoptosis and Autophagy: Current Understanding in Tick-Pathogen Interactions.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Cell death as part of innate immunity: Cause or consequence?Immunology · 2021Review
- Modulation of Cystatin C in Human Macrophages Improves Anti-Mycobacterial Immune Responses toFrontiers in immunology · 2021Article
- Structural and Evolutionary Adaptation of NOD-Like Receptors in Birds.BioMed research international · 2021Article
- Transcriptional Studies onFrontiers in cellular and infection microbiology · 2021Review
- Effect ofThe journal of venomous animals and toxins including tropical diseases · 2020Article
- The role of lysosome in regulated necrosis.Acta pharmaceutica Sinica. B · 2020Review
94 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Cryopyrin (CIAS1, NLRP3) and ASC are components of the inflammasome, a multiprotein complex required for caspase-1 activation and cytokine IL-1beta production. CIAS1 mutations underlie autoinflammation characterized by excessive IL-1beta secretion. Disease-associated cryopyrin also causes a program of necrosis-like cell death in macrophages, the mechanistic details of which are unknown. We find that patient monocytes carrying disease-associated CIAS1 mutations exhibit excessive necrosis-like death by a process dependent on ASC and cathepsin B, resulting in spillage of the proinflammatory mediator HMGB1. Shigella flexneri infection also causes cryopyrin-dependent macrophage necrosis with features similar to the death caused by mutant CIAS1. This necrotic death is independent of caspase-1 and IL-1beta, and thus independent of the inflammasome. Furthermore, necrosis of primary macrophages requires the presence of Shigella virulence genes. While similar proteins mediate pathogen-induced cell death in plants, this report identifies cryopyrin as an important host regulator of programmed pathogen-induced necrosis in animals, a process we term pyronecrosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.