ArticleEMBO reports2017
TLR3 downregulates expression of schizophrenia gene Disc1 via MYD88 to control neuronal morphology.
Article in EMBO reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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
32 citing papers in PubMed, 51 citations in OpenAlex.
- The association of the TLR3 SNP rs3775291 with schizophrenia is influenced by age.Frontiers in genetics · 2026Article
- The Role of Toll-like Receptor 3 Signaling in Cognitive Impairment Induced by Propofol Addiction.Molecular neurobiology · 2025Article
- Diverse Effects of Various Toll-Like Receptor 2 Ligands on Neuronal Activity and Cell Death.Cellular and molecular neurobiology · 2025Article
- Toll-like Receptors 1, 3 and 7 Activate Distinct Genetic Features of NF-κB Signaling and γ-Protocadherin Expression in Human Cardiac Fibroblasts.Inflammation · 2025Article
- MyD88 Contributes to TLR3-Mediated NF-κB Activation and Cytokine Production in Macrophages.Cells · 2025Article
- Nucleic acid sensing in the central nervous system: Implications for neural circuit development, function, and degeneration.Immunological reviews · 2024Review
- From Immunity to Neurogenesis: Toll-like Receptors as Versatile Regulators in the Nervous System.International journal of molecular sciences · 2024Review
- Toll-Like Receptor mRNA Levels in Schizophrenia: Association With Complement Factors and Cingulate Gyrus Cortical Thinning.Schizophrenia bulletin · 2024Article
- Early activation of Toll-like receptor-3 reduces the pathological progression of Alzheimer's disease in APP/PS1 mouse.Alzheimer's research & therapy · 2023Article
- Dual Role of the P2X7 Receptor in Dendritic Outgrowth during Physiological and Pathological Brain Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Unique Features of the Immune Response in BTBR Mice.International journal of molecular sciences · 2022Article
- Impact of SARS-CoV-2 on Host Factors Involved in Mental Disorders.Frontiers in microbiology · 2022Review
- Transcriptomic analysis of isolated and pooled human postmortem cerebellar Purkinje cells in autism spectrum disorders.Frontiers in genetics · 2022Article
- Article
- Innate immunity at the crossroads of healthy brain maturation and neurodevelopmental disorders.Nature reviews. Immunology · 2021Review
- Article
- Quantification of Dendritic Spines Remodeling under Physiological Stimuli and in Pathological Conditions.International journal of molecular sciences · 2021Review
- Transcriptomic Analysis and C-Terminal Epitope Tagging Reveal Differential Processing and Signaling of Endogenous TLR3 and TLR7.Frontiers in immunology · 2021Article
- KLHL17/Actinfilin, a brain-specific gene associated with infantile spasms and autism, regulates dendritic spine enlargement.Journal of biomedical science · 2020Article
- Microglial Density Alters Measures of Axonal Integrity and Structural Connectivity.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral infection during fetal or neonatal stages increases the risk of developing neuropsychiatric disorders such as schizophrenia and autism spectrum disorders. Although neurons express several key regulators of innate immunity, the role of neuronal innate immunity in psychiatric disorders is still unclear. Using cultured neurons and in vivo mouse brain studies, we show here that Toll-like receptor 3 (TLR3) acts through myeloid differentiation primary response gene 88 (MYD88) to negatively control Disrupted in schizophrenia 1 (Disc1) expression, resulting in impairment of neuronal development. Cytokines are not involved in TLR3-mediated inhibition of dendrite outgrowth. Instead, TLR3 signaling suppresses expression of several psychiatric disorder-related genes, including Disc1 The impaired dendritic arborization caused by TLR3 activation is rescued by MYD88 deficiency or DISC1 overexpression. In addition, TLR3 activation at the neonatal stage increases dendritic spine density, but narrows spine heads at postnatal day 21 (P21), suggesting a long-lasting effect of TLR3 activation on spinogenesis. Our study reveals a novel mechanism of TLR3 in regulation of dendritic morphology and provides an explanation for how environmental factors influence mental health.
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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.