Evidence map›Paper›PMID 21745188›Full record

ReviewClinical science (London, England : 1979)2011

Toll-like receptors in health and disease in the brain: mechanisms and therapeutic potential.

Mark L Hanke, Tammy Kielian

Open access · greenAbstract readReview
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed
12.7field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

226 citing papers in PubMed, 486 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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 · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
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  12. Crosstalk between MSC-extracellular vesicles andFrontiers in pharmacology · 2025
    Article
  13. Review
  14. Review
  15. Modeling extrahepatic hepatitis E virus infection in induced human primary neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

166 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Mark L HankeDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Tammy Kielian
University of Nebraska Medical Center · US

Funding

THE PATHOGENESIS OF BRAIN ABSCESSR01NS040730 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI KIELIAN, TAMMY L · 2001 to 2013
$3.4M
Effects of Neuroinflammation on Gap Junction Communication in GliaR01NS053487 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI KIELIAN, TAMMY L · 2006 to 2010
$1.4M
Receptors Involved in Microglial Responses to S. aureusR01MH065297 · NIMH · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI KIELIAN, TAMMY L · 2002 to 2005
$1.2M
Receptors Involved in Microglial Responses to S. aureusR01NS055385 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI KIELIAN, TAMMY L · 2007 to 2010
$1.1M
NIMH NIH HHS R01 MH065297NINDS NIH HHS R01 NS040730NINDS NIH HHS R01 NS053487NINDS NIH HHS R01 NS055385
6 · The paper itself

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.

Indexed as

Alzheimer DiseaseAnimalsAstrocytesBrainBrain DiseasesCentral Nervous SystemHumansImmunity, InnateLearningMemoryMeningitis, BacterialMiceMicrogliaModels, BiologicalNeurogenesisNeuronsToll-Like Receptors

Identifiers

PMID21745188
PMCPMC4231819
OpenAlexW2121347099

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.