Cited by 203Inflammasome and immune disordersImmune Response and InflammationNeuroinflammation and Neurodegeneration Mechanisms

Toll-like receptor (TLR) and inflammasome actions in the central nervous system

Open access
Hanamsagar, Richa, Hanke, Mark L., Kielian, Tammy·2012·Trends in Immunology

Abstract

During the past 10 years, much attention has been focused towards elucidating the impact of Toll-like receptors (TLRs) in central nervous system (CNS) innate immunity. TLR signaling triggers the transcriptional activation of pro-interleukin-1β (pro-IL-1β) and pro-IL-18 that are processed into their active forms by the inflammasome. Recent studies have demonstrated inflammasome involvement during CNS infection, autoimmune disease, and injury. This review will address inflammasome actions within the CNS and how cooperation between TLR and inflammasome signaling may influence disease outcome. In addition, the concept of alternative inflammasome functions independent of IL-1 and IL-18 processing are considered in the context of CNS disease.

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.it.2012.03.001

Cites

106 of 106 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?

  • Signaling at TLR2 and TLR4 initiates an NF-κB-dependent signaling cascade that transcribes pro-IL-1β and NLRP3.

    “Importantly, signaling at TLR2 and TLR4 initiates an NF-κB-dependent signaling cascade that transcribes pro-IL-1β and NLRP3 (Hanamsagar et al, 2012).”

    From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Hanamsagar et al, 2012

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

Research works printed but not linked: 1

  1. [83]Lim JE MyD88 Deficiency Ameliorates beta-Amyloidosis in an Animal Model of Alzheimer's Disease Am J Pathol 2011 PMC3157279 21763676

Cited by

Sorted by citations

Authors
Hanamsagar, R., Hanke, M. L., & Kielian, T.
Affiliations
University of Nebraska Medical Center (US)
Corresponding author
Kielian, Tammy
Venue
Trends in Immunology
Publisher
Elsevier BV
Published
2012-07
Volume
33
Issue
7
Pages
333-342
ISSN
1471-4906 (ISSN-L)
OpenAlex
W2035824519
Cited by
203
References
106
Citations by year
2026: 3 · 2025: 14 · 2024: 11 · 2023: 7 · 2022: 15 · 2021: 17 · 2020: 10 · 2019: 14 · 2018: 12 · 2017: 15 · 2016: 18 · 2015: 17 · 2014: 24 · 2013: 24 · 2012: 2
FWCI
1.95
Type
journal article
Language
en
Open access
Locations
  • Trends in Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • University of Nebraska Medical Center
  • National Institute of Neurological Disorders and Stroke (R01NS055385, R01NS040730, R01NS053487, NS053487)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Toll-like receptors, inflammasome, central nervous system, innate immunity, IL-1β, IL-18, neuroinflammation, central nervous system infection, autoimmune disease, central nervous system injury
MeSH terms
Animals, Central Nervous System, Humans, Signal Transduction, Autoimmunity, Toll-Like Receptors, Inflammasomes

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