ArticleImmunity2009
A mutation in the Nlrp3 gene causing inflammasome hyperactivation potentiates Th17 cell-dominant immune responses.
Article in Immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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.
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Who cites it
185 citing papers in PubMed, 1 synthesis or guideline pooled it, 361 citations in OpenAlex.
- Prognostic significance of NLRP-3 expression in solid cancers: a systematic review and meta-analysis.Annals of medicine · 2026Pooled it
- Pathogenic NLRP3 mutants form constitutively active inflammasomes resulting in immune-metabolic limitation of IL-1β production.Nature communications · 2024Trial
- The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2017Trial
- Vascular smooth muscle-specific NLRP3 hyperactivation exacerbates arterial intimal hyperplasia in mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- The Multifaceted Roles of Macrophages in Rheumatoid Arthritis: From Cytokine Networks to the Discovery of Novel Subsets.International journal of molecular sciences · 2026Review
- TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.Nature communications · 2026Article
- Mice humanized by syntenic replacement with full-length NLRP3 disease-associated variants model the clinical cryopyrinopathy continuum.JCI insight · 2026Article
- Sex dictates IL-17A regulation: Inflammatory determinants in males versus a potassium-linked metabolic axis in females.PloS one · 2026Article
- NLRP3 inflammasome and hearing loss: from mechanisms to therapies.Journal of neuroinflammation · 2025Review
- Novel Insights into the Clinical Features, Genetic Spectrum and Clonal Evolution of Patients Carrying NLRP3 Mosaicism.Journal of clinical immunology · 2025Article
- Signal-induced NLRP3 phase separation initiates inflammasome activation.Cell research · 2025Article
- Review
- Decoding Immunobiology Through Genetic Errors of Immunity.Annual review of immunology · 2025Review
- The Role of IL-17 in Systemic Autoinflammatory Diseases: Mechanisms and Therapeutic Perspectives.Clinical reviews in allergy & immunology · 2025Review
- Anti-Cytokine Active Immunotherapy Based on Supramolecular Peptides for Alleviating IL-1β-Mediated Inflammation.Advanced healthcare materials · 2025Article
- Adult-Onset Still's Disease (AOSD)-On the Basis of Own Cases.Biomedicines · 2024Article
- Cell death as an architect of adult skin stem cell niches.Cell death and differentiation · 2024Review
- Article
- Anti-inflammatory effect of Trichospira verticillata via suppression of the NLRP3 inflammasome in neutrophilic asthma.Journal of cellular and molecular medicine · 2024Article
- The discovery of NLRP3 and its function in cryopyrin-associated periodic syndromes and innate immunity.Immunological reviews · 2024Review
125 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Missense mutations of the gene encoding NLRP3 are associated with autoinflammatory disorders characterized with excessive production of interleukin-1beta (IL-1beta). Here we analyzed the immune responses of gene-targeted mice carrying a mutation in the Nlrp3 gene equivalent to the human mutation associated with Muckle-Wells Syndrome. We found that antigen-presenting cells (APCs) from such mice produced massive amounts of IL-1beta upon stimulation with microbial stimuli in the absence of ATP. This was likely due to a diminished inflammasome activation threshold that allowed a response to the small amount of agonist. Moreover, the Nlrp3 gene-targeted mice exhibited skin inflammation characterized by neutrophil infiltration and a Th17 cytokine-dominant response, which originated from hematopoietic cells. The inflammation of Nlrp3 gene-targeted mice resulted from excess IL-1beta production from APCs, which augmented Th17 cell differentiation. These results demonstrate that the NLRP3 mutation leads to inflammasome hyperactivation and consequently Th17 cell-dominant immunopathology in autoinflammation.
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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.