ArticleCell2012
TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by gram-negative bacteria.
Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 463 papers.
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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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Who cites it
463 citing papers in PubMed, 711 citations in OpenAlex.
- A Novel Biofilm Amyloid Ligand for Caspase-11 Drives Hyperactivation in Dendritic Cells.bioRxiv : the preprint server for biology · 2026Article
- When folding CARDs wins the game: molecular snapshots of lipopolysaccharide sensing by the non-canonical inflammasome.Biochemical Society transactions · 2026Review
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Intestinal Flora and Myocarditis: Potential Mechanisms and Therapeutic Strategies Affecting Disease Progression and Cardiac Function.International journal of molecular sciences · 2026Review
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- Mapping the holonomic signaling network that drives pathological changes in endotoxic shock.Cellular & molecular immunology · 2026Article
- Differential Host Gene Expression Associated with Non-Research square · 2026Article
- GTPase Rab11b and effector Rab11-FIP2 promote NLRP3 stability during inflammasome priming.The EMBO journal · 2026Article
- Conservation of NLRP3 Inflammasome Pathway in Monotremes and Large-Scale Restructuring of the Caspase-1 Gene Cluster Region in Mammals.Journal of molecular evolution · 2026Article
- Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer's disease retina.Nature communications · 2026Article
- Extracellular Lipopolysaccharide Triggers the Release of Unconjugated Interferon-Stimulated Gene 15 (ISG15) Protein from Macrophages via Type-I Interferon/Caspase-4/Gasdermin-D Pathway.Pathogens (Basel, Switzerland) · 2026Article
- Environmental Amino Acid Sensing Regulates the Rate of ASC Translation and NLRP3 Inflammasome Assembly.bioRxiv : the preprint server for biology · 2026Article
- P2X7 receptor contributes to hepatic inflammation and collagen deposition in methionine- and choline-deficient diet-fed mice.Frontiers in pharmacology · 2026Article
- Neutrophil extracellular traps in diabetic wound healing: mechanisms, pathological roles, and therapeutic implications.Burns & trauma · 2026Review
- Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026Review
- Pharmacological intervention of the HMGB1-pCTS-L axis to ameliorate inflammatory diseases.Frontiers in immunology · 2026Review
- Geranylgeranoic acid, toll-like receptor 4, and pyroptosis-related signaling in hepatocellular carcinoma: a hypothesis-generating perspective.Oncology reviews · 2026Article
- Convergent death programs in chronic obstructive pulmonary disease: how pyroptotic and ferroptotic crosstalk reshapes therapeutic paradigms.Frontiers in immunology · 2026Review
- Advances of Caspase-11 for veterinary respiratory infections.Frontiers in veterinary science · 2026Review
- Gut bacteria-derived sphingolipids alter innate immune responses to oral cholera vaccine antigens.Nature communications · 2025Article
403 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Systemic infections with Gram-negative bacteria are characterized by high mortality rates due to the "sepsis syndrome," a widespread and uncontrolled inflammatory response. Though it is well recognized that the immune response during Gram-negative bacterial infection is initiated after the recognition of endotoxin by Toll-like receptor 4, the molecular mechanisms underlying the detrimental inflammatory response during Gram-negative bacteremia remain poorly defined. Here, we identify a TRIF pathway that licenses NLRP3 inflammasome activation by all Gram-negative bacteria. By engaging TRIF, Gram-negative bacteria activate caspase-11. TRIF activates caspase-11 via type I IFN signaling, an event that is both necessary and sufficient for caspase-11 induction and autoactivation. Caspase-11 subsequently synergizes with the assembled NLRP3 inflammasome to regulate caspase-1 activation and leads to caspase-1-independent cell death. These events occur specifically during infection with Gram-negative, but not Gram-positive, bacteria. The identification of TRIF as a regulator of caspase-11 underscores the importance of TLRs as master regulators of inflammasomes during Gram-negative bacterial infection.
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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.