ArticleThe Journal of clinical investigation2016
NLRP3 tyrosine phosphorylation is controlled by protein tyrosine phosphatase PTPN22.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 133 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.
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
133 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.
- The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.Cell communication and signaling : CCS · 2025Pooled it
- Loss-of-function CARD8 mutation causes NLRP3 inflammasome activation and Crohn's disease.The Journal of clinical investigation · 2018Trial
- Inhibition of ERK5 activity ameliorates osteoarthritis by suppressing NLRP3 inflammasome-mediated chondrocyte pyroptosis.Bone research · 2026Article
- A Review on Structural Insights into NLRP3 and NEK7: Domain Architecture, Subcellular Localization, and Their Interaction in Inflammasome Assembly and Signaling.Molecular neurobiology · 2026Review
- Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026Review
- Inflammasome adaptor protein ASC is a mechanistic checkpoint in IL-1β maturation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Indirect inhibition of the NLRP3-interleukin-1β axis contributes to the efficacy of JAK1 inhibitors in experimental colitis and human ulcerative colitis.Nature communications · 2026Article
- An autoimmunity-associated allele ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Post-translational modifications of NLRP3: to prime or not to prime?Trends in immunology · 2026Review
- PTPN22 as a therapeutic target in intervertebral disc degeneration: Modulating mitophagy and pyroptosis through the PI3K/AKT/mTOR axis.Journal of advanced research · 2026Article
- APIP regulates the priming of canonical NLRP3 and non-canonical Caspase-11/4 inflammasomes by binding to TRAF6.Nature communications · 2025Article
- An Autoimmunity-associated allele ofbioRxiv : the preprint server for biology · 2025Article
- Nitroxoline is a novel inhibitor of NLRP3-dependent pyroptosis.Cell death discovery · 2025Article
- CircGTF2H2C Regulates NLRP3 Dephosphorylation via Modulating PTPN11 Expression in Spinal Cord Injury.Molecular neurobiology · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- The desulfinylation enzyme sulfiredoxin-1 attenuates HSC activation and liver fibrosis by modulating the PTPN12-NLRP3 axis.Hepatology (Baltimore, Md.) · 2025Article
- Inflammasome Signaling in Cardiac Arrhythmias: Linking Inflammation, Fibrosis, and Electrical Remodeling.International journal of molecular sciences · 2025Review
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Mechanisms of NLRP3 activation and inhibition elucidated by functional analysis of disease-associated variants.Nature immunology · 2025Article
- Intestinal epithelial PTPN23 is essential for gut barrier integrity and prevention of fatal bacterial translocation.Journal of Crohn's & colitis · 2025Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes form as the result of the intracellular presence of danger-associated molecular patterns and mediate the release of active IL-1β, which influences a variety of inflammatory responses. Excessive inflammasome activation results in severe inflammatory conditions, but physiological IL-1β secretion is necessary for intestinal homeostasis. Here, we have described a mechanism of NLRP3 inflammasome regulation by tyrosine phosphorylation of NLRP3 at Tyr861. We demonstrated that protein tyrosine phosphatase non-receptor 22 (PTPN22), variants in which are associated with chronic inflammatory disorders, dephosphorylates NLRP3 upon inflammasome induction, allowing efficient NLRP3 activation and subsequent IL-1β release. In murine models, PTPN22 deficiency resulted in pronounced colitis, increased NLRP3 phosphorylation, but reduced levels of mature IL-1β. Conversely, patients with inflammatory bowel disease (IBD) that carried an autoimmunity-associated PTPN22 variant had increased IL-1β levels. Together, our results identify tyrosine phosphorylation as an important regulatory mechanism for NLRP3 that prevents aberrant inflammasome activation.
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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.