ArticleDisease models & mechanisms2024
The NLRP3 inflammasome is essential for IL-18 production in a murine model of macrophage activation syndrome.
Article in Disease models & mechanisms, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- The value of C-X-C motif chemokine ligand 9 (CXCL9) in the differential diagnosis and management of haemophagocytic lymphohistiocytosis.British journal of haematology · 2026Article
- Disruption of macrophage cell volume drives inflammatory responses and type I interferon signaling.The Journal of cell biology · 2026Article
- 3D Artificial Skin Model As a Novel Strategy for the Detection of Pyroptosis-Cascade Activation in Amyotrophic Lateral Sclerosis.ACS applied materials & interfaces · 2026Article
- IL-18-Mediated Tumor Immune Evasion.Current issues in molecular biology · 2026Review
- Cytokine storm.Nature reviews. Disease primers · 2026Review
- Pattern recognition receptor signaling in otitis media: immune crosstalk and pathogenic mechanisms.Frontiers in immunology · 2026Review
- NLRP3 inflammasome-driven hemophagocytic lymphohistiocytosis occurs independent of IL-1β and IL-18 and is targetable by BET inhibitors.Science advances · 2025Article
- Inflammasomes in Cardiovascular Diseases: Current Knowledge and Future Perspectives.International journal of molecular sciences · 2025Review
- Death as rebirth: how efferocytosis drives tissue repair and disease treatment.Frontiers in immunology · 2025Review
- Early identification of macrophage activation syndrome in adult-onset Still's disease: a case report and literature review.Frontiers in medicine · 2025Article
- An improved understanding of pediatric chronic nonbacterial osteomyelitis pathophysiology informs current and future treatment.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Review
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Abstract
Hyperinflammatory disease is associated with an aberrant immune response resulting in cytokine storm. One such instance of hyperinflammatory disease is known as macrophage activation syndrome (MAS). The pathology of MAS can be characterised by significantly elevated serum levels of interleukin-18 (IL-18) and interferon gamma (IFNγ). Given the role for IL-18 in MAS, we sought to establish the role of inflammasomes in the disease process. Using a murine model of CpG-oligonucleotide-induced MAS, we discovered that the expression of the NLRP3 inflammasome was increased and correlated with IL-18 production. Inhibition of the NLRP3 inflammasome or the downstream caspase-1 prevented MAS-mediated upregulation of IL-18 in the plasma but, interestingly, did not alleviate key features of hyperinflammatory disease including hyperferritinaemia and splenomegaly. Furthermore blockade of IL-1 receptor with its antagonist IL-1Ra did not prevent the development of CpG-induced MAS, despite being clinically effective in the treatment of MAS. These data demonstrate that, during the development of MAS, the NLRP3 inflammasome was essential for the elevation in plasma IL-18 - a key cytokine in clinical cases of MAS - but was not a driving factor in the pathogenesis of CpG-induced MAS.
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