ReviewClinical science (London, England : 1979)2011
Toll-like receptors in health and disease in the brain: mechanisms and therapeutic potential.
Review in Clinical science (London, England : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers.
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
226 citing papers in PubMed, 486 citations in OpenAlex.
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- IMMUND: A Diagnostic and Therapeutic Pipeline to Uncover the Convergence in Functional Perturbation at Early Stages of Neurodegenerative Diseases and Multiple Sclerosis Based on Protein Markers.International journal of molecular sciences · 2026Article
- Inflammation and treatment strategies for suicidal behavior.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2026Review
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- Differential Responses of Human iPSC-Derived Microglia to Stimulation with Diverse Inflammogens.Cells · 2025Article
- MicroRNAs in the biology and hallmarks of neurodegenerative diseases.Trends in molecular medicine · 2025Review
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- Ergolide Regulates Microglial Activation and Inflammatory-Mediated Dysfunction: A Role for the Cysteinyl Leukotriene Pathway.International journal of molecular sciences · 2025Article
- Cognitive Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome-Aetiology and Potential Treatments.International journal of molecular sciences · 2025Review
- Role of toll-like receptors in post-COVID-19 associated neurodegenerative disorders?Frontiers in medicine · 2025Review
- Crosstalk between MSC-extracellular vesicles andFrontiers in pharmacology · 2025Article
- Pharmacological mechanisms and potential clinical applications of Dihydromyricetin in neurological disorders.Frontiers in pharmacology · 2025Review
- Review of the mechanism of infection induced cerebral small vessel disease.Frontiers in immunology · 2025Review
- Modeling extrahepatic hepatitis E virus infection in induced human primary neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Exploring the Role of Apigenin in Neuroinflammation: Insights and Implications.International journal of molecular sciences · 2024Review
- Neuroactive Steroids, Toll-like Receptors, and Neuroimmune Regulation: Insights into Their Impact on Neuropsychiatric Disorders.Life (Basel, Switzerland) · 2024Review
- Review
- Review
- miR-154-5p Is a Novel Endogenous Ligand for TLR7 Inducing Microglial Activation and Neuronal Injury.Cells · 2024Article
166 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 discovery of mammalian TLRs (Toll-like receptors), first identified in 1997 based on their homology with Drosophila Toll, greatly altered our understanding of how the innate immune system recognizes and responds to diverse microbial pathogens. TLRs are evolutionarily conserved type I transmembrane proteins expressed in both immune and non-immune cells, and are typified by N-terminal leucine-rich repeats and a highly conserved C-terminal domain termed the TIR [Toll/interleukin (IL)-1 receptor] domain. Upon stimulation with their cognate ligands, TLR signalling elicits the production of cytokines, enzymes and other inflammatory mediators that can have an impact on several aspects of CNS (central nervous system) homoeostasis and pathology. For example, TLR signalling plays a crucial role in initiating host defence responses during CNS microbial infection. Furthermore, TLRs are targets for many adjuvants which help shape pathogen-specific adaptive immune responses in addition to triggering innate immunity. Our knowledge of TLR expression and function in the CNS has greatly expanded over the last decade, with new data revealing that TLRs also have an impact on non-infectious CNS diseases/injury. In particular, TLRs recognize a number of endogenous molecules liberated from damaged tissues and, as such, influence inflammatory responses during tissue injury and autoimmunity. In addition, recent studies have implicated TLR involvement during neurogenesis, and learning and memory in the absence of any underlying infectious aetiology. Owing to their presence and immune-regulatory role within the brain, TLRs represent an attractive therapeutic target for numerous CNS disorders and infectious diseases. However, it is clear that TLRs can exert either beneficial or detrimental effects in the CNS, which probably depend on the context of tissue homoeostasis or pathology. Therefore any potential therapeutic manipulation of TLRs will require an understanding of the signals governing specific CNS disorders to achieve tailored therapy.
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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.