Cited by 490Neuroinflammation and Neurodegeneration MechanismsImmune Response and InflammationInflammasome and immune disorders

Pattern recognition receptors and central nervous system repair

Open access
Kigerl, Kristina A., de Rivero Vaccari, Juan Pablo, Dietrich, W. Dalton, Popovich, Phillip G., Keane, Robert W.·2014·Experimental Neurology

Abstract

Pattern recognition receptors (PRRs) are part of the innate immune response and were originally discovered for their role in recognizing pathogens by ligating specific pathogen associated molecular patterns (PAMPs) expressed by microbes. Now the role of PRRs in sterile inflammation is also appreciated, responding to endogenous stimuli referred to as "damage associated molecular patterns" (DAMPs) instead of PAMPs. The main families of PRRs include Toll-like receptors (TLRs), Nod-like receptors (NLRs), RIG-like receptors (RLRs), AIM2-like receptors (ALRs), and C-type lectin receptors. Broad expression of these PRRs in the CNS and the release of DAMPs in and around sites of injury suggest an important role for these receptor families in mediating post-injury inflammation. Considerable data now show that PRRs are among the first responders to CNS injury and activation of these receptors on microglia, neurons, and astrocytes triggers an innate immune response in the brain and spinal cord. Here we discuss how the various PRR families are activated and can influence injury and repair processes following CNS injury.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.expneurol.2014.01.001

Cites

144 of 144 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Because TLR3 is abundantly expressed in the brain, abnormal activation of NMDA receptor signalling by quinolinic acid might be at least partially responsible for numerous neurological diseases.

    “As TLR3 is abundantly expressed in the brain187, abnormal activation of NMDA receptor signalling by quinolinic acid might be at least partially responsible for numerous neurological diseases186,188.”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Kigerl, K. A., de Rivero Vaccari, J. P., Dietrich, W. D., Popovich, P. G., & Keane, R. W.
Affiliations
  • The Ohio State University Wexner Medical Center (US)
  • University of Miami (US)
Corresponding author
  • Popovich, Phillip G.
  • Keane, Robert W.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2014-08
Volume
258
Pages
5-16
ISSN
0014-4886 (ISSN-L)
OpenAlex
W2031080649
Cited by
490
References
143
Citations by year
2026: 26 · 2025: 44 · 2024: 44 · 2023: 50 · 2022: 59 · 2021: 50 · 2020: 50 · 2019: 38 · 2018: 38 · 2017: 38 · 2016: 15 · 2015: 31 · 2014: 6
FWCI
2.44
Type
journal article
Language
en
Open access
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Neurological Disorders and Stroke (NS-043246, R01NS042133, NS059836, R01NS059836, R01NS043246)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
pattern recognition receptors, central nervous system injury, neuroinflammation, damage-associated molecular patterns, pathogen-associated molecular patterns, Toll-like receptors, NOD-like receptors, RIG-I-like receptors, AIM2-like receptors, C-type lectin receptors, microglia, astrocytes, neurons, CNS repair, innate immunity
MeSH terms
Animals, Cell Survival, Central Nervous System Diseases, Humans, Immunity, Innate, Signal Transduction, Receptors, Pattern Recognition, Toll-Like Receptors

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review