ArticleNature2011
The NLRC4 inflammasome receptors for bacterial flagellin and type III secretion apparatus.
Article in Nature, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 766 papers, 1 of them a synthesis that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
766 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,242 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
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- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- Innate immune sensors of inflammasomes and PANoptosomes: structural-mechanistic insights and therapeutic implications.Cell research · 2026Review
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- Malvidin-3-O-Rhamnoside Alleviates Klebsiella pneumoniae -Induced Acute Lung Injury by Regulating Macrophage-Mediated Inflammatory and Oxidative Pathways.Phytotherapy research : PTR · 2026Article
- OmpW-mediated sensing of MUC2 GalNAc contributes to the ileal tropism of Salmonella Typhi.Cell reports · 2026Article
- Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Pyroptosis: Molecular mechanisms and function.Journal of physiology and biochemistry · 2026Review
- The Co-Evolutionary Arms Race BetweenMicroorganisms · 2026Review
- Temperate phages enhance bacterial host fitness via RNA-guided flagellar remodelling.Nature microbiology · 2026Article
- Threat assessment shapes neutrophil cell fate upon inflammasome activation.Science advances · 2026Article
- NLR Inflammasomes in Viral Infections: From Molecular Mechanisms to Therapeutic Interventions.Viruses · 2026Review
- A derivative of PD156707 selectively inhibits NLRP3 inflammasome activation by directly binding to NLRP3.Scientific reports · 2026Article
- An overview of human inflammasomes: Activation and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Pathogen hijacks focal adhesion signaling by a T3SS effector CteX.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Many but not all pathogen-associated molecular patterns aggravate neurogenic heterotopic ossification after spinal cord injury.Journal of biomedical science · 2026Article
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- Role of Nod-like Receptors inMicroorganisms · 2026Review
- Article
706 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes are large cytoplasmic complexes that sense microbial infections/danger molecules and induce caspase-1 activation-dependent cytokine production and macrophage inflammatory death. The inflammasome assembled by the NOD-like receptor (NLR) protein NLRC4 responds to bacterial flagellin and a conserved type III secretion system (TTSS) rod component. How the NLRC4 inflammasome detects the two bacterial products and the molecular mechanism of NLRC4 inflammasome activation are not understood. Here we show that NAIP5, a BIR-domain NLR protein required for Legionella pneumophila replication in mouse macrophages, is a universal component of the flagellin-NLRC4 pathway. NAIP5 directly and specifically interacted with flagellin, which determined the inflammasome-stimulation activities of different bacterial flagellins. NAIP5 engagement by flagellin promoted a physical NAIP5-NLRC4 association, rendering full reconstitution of a flagellin-responsive NLRC4 inflammasome in non-macrophage cells. The related NAIP2 functioned analogously to NAIP5, serving as a specific inflammasome receptor for TTSS rod proteins such as Salmonella PrgJ and Burkholderia BsaK. Genetic analysis of Chromobacterium violaceum infection revealed that the TTSS needle protein CprI can stimulate NLRC4 inflammasome activation in human macrophages. Similarly, CprI is specifically recognized by human NAIP, the sole NAIP family member in human. The finding that NAIP proteins are inflammasome receptors for bacterial flagellin and TTSS apparatus components further predicts that the remaining NAIP family members may recognize other unidentified microbial products to activate NLRC4 inflammasome-mediated innate immunity.
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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.