ReviewInternational immunology2018
Novel aspects of the assembly and activation of inflammasomes with focus on the NLRC4 inflammasome.
Review in International immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Innate immune sensors of inflammasomes and PANoptosomes: structural-mechanistic insights and therapeutic implications.Cell research · 2026Review
- Importance of the inflammasome in gut-brain axis: from pathological driver to therapeutic target.Inflammopharmacology · 2026Review
- FoxO1 promotes high glucose-induced inflammation and cataract formation via JAK1/STAT1.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025Article
- Baicalein Suppresses NLRP3 and AIM2 Inflammasome-Mediated Pyroptosis in Macrophages Infected by Mycobacterium tuberculosis via Induced Autophagy.Microbiology spectrum · 2023Article
- Prognostic significance of serum NLRC4 in patients with acute supratentorial intracerebral hemorrhage: A prospective longitudinal cohort study.Frontiers in neurology · 2023Article
- Optimization of cancer immunotherapy through pyroptosis: A pyroptosis-related signature predicts survival benefit and potential synergy for immunotherapy in glioma.Frontiers in immunology · 2022Article
- A Prognostic Signature Consisting of Pyroptosis-Related Genes and SCAF11 for Predicting Immune Response in Breast Cancer.Frontiers in medicine · 2022Article
- Inflammasome and Its Therapeutic Targeting in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- SIRT3-mediated deacetylation of NLRC4 promotes inflammasome activation.Theranostics · 2021Article
- ATP-Binding and Hydrolysis in Inflammasome Activation.Molecules (Basel, Switzerland) · 2020Review
- The effects of NLRP3 inflammasome inhibition by MCC950 on LPS-induced pancreatic adenocarcinoma inflammation.Journal of cancer research and clinical oncology · 2020Article
- Key Components of Inflammasome and Pyroptosis Pathways Are Deficient in Canines and Felines, Possibly Affecting Their Response to SARS-CoV-2 Infection.Frontiers in immunology · 2020Article
- Distinct Roles of IL-1β and IL-18 in NLRC4-Induced Autoinflammation.Frontiers in immunology · 2020Article
- Single-Center Overview of Pediatric Monogenic Autoinflammatory Diseases in the Past Decade: A Summary and Beyond.Frontiers in immunology · 2020Article
- Human Autoinflammatory Diseases Mediated by NLRP3-, Pyrin-, NLRP1-, and NLRC4-Inflammasome Dysregulation Updates on Diagnosis, Treatment, and the Respective Roles of IL-1 and IL-18.Frontiers in immunology · 2020Review
- Introduction: Autoinflammatory Syndromes Special Issue-hidden mysteries in the corners of autoinflammation.International immunology · 2018Article
- A Study of NLRC4 in Patients with Leprosy.Indian journal of dermatologyArticle
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Inflammasomes are multiprotein structures that activate caspase-1, support secretion of pro-inflammatory cytokines, IL-1β and IL-18, and also induce inflammatory programmed cell death, termed pyoptosis. Inflammasomes are activated in response to the detection of endogenous and microbially derived danger signals and are mediated by several classes of inflammasome-forming sensors. These include several nucleotide-binding proteins of the NOD-like receptor (NLR) family, including NLRP1, NLRP3 and NLRC4, as well as the proteins Absent in Melanoma 2 (AIM2) and Pyrin. Mutations in genes encoding some of these sensors have been found to be associated with gain-of-function monogenetic inflammatory disorders in humans. Genetic, biochemical and structural studies have begun to demonstrate how these proteins sense danger signals and to shed light on the step-by-step processes that are necessary for the assembly of inflammasomes, in both physiologic responses to pathogens and potentially in autoinflammatory conditions. Recent biochemical studies of pro-caspase-1 and an adapter protein known as ASC suggest that inflammasomes act to initiate self-generating effector filaments responsible for activating caspase-1 and initiating downstream signaling. These studies have suggested a model of molecular events from sensor activation to inflammasome formation that may describe processes that are universal to inflammasome formation.
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