ReviewBrain, behavior, and immunity2018
Principles of inflammasome priming and inhibition: Implications for psychiatric disorders.
Review in Brain, behavior, and immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Immunological landscape of nanotechnology-based depression research: a bibliometric analysis of neuroinflammation and immune modulation.Frontiers in immunology · 2026Pooled it
- The NLRP3 inflammasome: pathophysiology and therapeutic implications for schizophrenia and neuropsychiatric disorders.Molecular psychiatry · 2026Review
- Alcohol drinking sex-dependently regulates interleukin-1 pro-inflammatory signaling in the prefrontal cortex of mice and rhesus macaques.Brain, behavior, and immunity · 2026Article
- King Oyster Mushroom,Nutrients · 2026Article
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Caspase-8-mediated CYLD cleavage boosts LPS-induced endotoxic shock.Cell death and differentiation · 2026Article
- Serum Amyloid A-Dependent Inflammasome Activation and Acute Injury in a Mouse Model of Experimental Stroke.International journal of molecular sciences · 2026Article
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- Role of Dietary Polyphenols in NAD+-Dependent Deacetylase SIRT 1 in Stress-Induced Depression.Molecular neurobiology · 2025Review
- Associations of serum TNF-α, IL-8, and IL-18 levels with the clinical symptoms in acute schizophrenia: a cross-sectional study.BMC psychiatry · 2025Article
- Neurometabolomic impacts of wood smoke and protective benefits of anti-aging therapeutics in aged female C57BL/6J mice.Particle and fibre toxicology · 2025Article
- Progress in targeting the NLRP3 signaling pathway for inflammatory bowel disease (Review).Molecular medicine reports · 2025Review
- Recent Advances and Future Directions in Alzheimer's Disease Genetic Research.International journal of molecular sciences · 2025Review
- Neohesperidin Improves Depressive-Like Behavior Induced by Chronic Unpredictable Mild Stress in Mice.Neurochemical research · 2025Article
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- Jiannao Pills alleviate depression-like behavior in chronic unpredictable mild stress-induced mice through NF-κB/NLRP3 pathway.Frontiers in pharmacology · 2025Article
- The risk for psychiatric disorders in offspring from thrombosis-prone pedigrees in Sweden: a nationwide family study.Research and practice in thrombosis and haemostasis · 2025Article
- Anti-depressant effect of Naringenin-loaded hybridized nanoparticles in diabetic rats via PPARγ/NLRP3 pathway.Scientific reports · 2024Article
- Type I interferon regulates interleukin-1beta and IL-18 production and secretion in human macrophages.Life science alliance · 2024Article
- Sera from people with HIV and depression induce commensurate metabolic alterations in astrocytes: toward precision diagnoses and therapies.NeuroImmune pharmacology and therapeutics · 2024Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The production of inflammatory proteins by the innate immune system is a tightly orchestrated procedure that allows the body to efficiently respond to exogenous and endogenous threats. Recently, accumulating evidence has indicated that disturbances in the inflammatory response system not only provoke autoimmune disorders, but also can have deleterious effects on neuronal function and mental health. As inflammation in the brain is primarily mediated by microglia, there has been an expanding focus on the mechanisms through which these cells initiate and propagate neuroinflammation. Microglia can enter persistently active states upon their initial recognition of an environmental stressor and are thereafter prone to elicit amplified and persistent inflammatory responses following subsequent exposures to stressors. A recent focus on why primed microglia cells are susceptible to environmental insults has been the NLRP3 inflammasome. Its function within the innate immune system is regulated in such a manner that supports a role for the complex in gating neuroinflammatory responses. The activation of NLRP3 inflammasome in microglia results in the cleavage of zymogen inflammatory interleukins into functional forms that elicit a number of consequential effects in the local neuronal environment. There is evidence to support the principle that within primed neuroimmune systems a lowered threshold for NLRP3 activation can cause persistent neuroinflammation or the amplified production of inflammatory cytokines, such as IL-1β and IL-18. Over the course of an individual's lifetime, persistent neuroinflammation can subsequently lead to the pathophysiological signatures that define psychological disorders. Therefore, targeting the NLRP3 inflammasome complex may represent an innovative and consequential approach to limit neuroinflammatory states in psychiatric disorders, such as major depressive disorder.
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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.