Evidence map›Paper›PMID 31612243›Full record

ReviewSeminars in immunopathology2019

An emerging role for Toll-like receptors at the neuroimmune interface in osteoarthritis.

Rachel E Miller, Carla R Scanzello, Anne-Marie Malfait

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  18. HU308 Mitigates Osteoarthritis by Stimulating Sox9-Related Networks of Carbohydrate Metabolism.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Article
  19. Article
  20. Lysophosphatidylcholine: Potential Target for the Treatment of Chronic Pain.International journal of molecular sciences · 2022
    Review
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

3 authors at 2 institutions in 1 country.

Rachel E MillerDivision of Rheumatology, Department of Internal Medicine, Rush University Medical Center, 1611 W Harrison Street, Chicago, IL, 60612, USA.ORCID 0000-0002-4486-5757
Carla R ScanzelloSection of Rheumatology and Translational Musculoskeletal Research Center, Corporal Michael J. Crescenz Veterans Affairs Medical Center & Division of Rheumatology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.ORCID 0000-0002-9290-188X
Anne-Marie MalfaitDivision of Rheumatology, Department of Internal Medicine, Rush University Medical Center, 1611 W Harrison Street, Chicago, IL, 60612, USA. anne-marie_malfait@rush.edu.ORCID 0000-0003-1428-0384
Rush University Medical Center · USUniversity of Pennsylvania · US

Funding

Osteoarthritis Progression And Sensory Pathway AlterationsR01AR064251 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MALFAIT, ANNE-MARIE, MILLER, RICHARD J · 2013 to 2025
$7.6M
Molecular Pathways of Pain Generation in OsteoarthritisR01AR060364 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MALFAIT, ANNE-MARIE · 2011 to 2025
$6.0M
Biomechanical Pathways Associated with Osteoarthritis PainK01AR070328 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MILLER, RACHEL ELIZABETH · 2016 to 2020
$547k
The Impact of C-C Chemokine Receptor 7 (CCR7) on Synovitis and Osteoarthritis (OA)I21RX001757 · VA · PHILADELPHIA VA MEDICAL CENTER · PI SCANZELLO, CARLA ROSE · 2015 to 2018
–
NIAMS NIH HHS K01 AR070328NIAMS NIH HHS R01 AR060364NIAMS NIH HHS R01 AR064251RRD VA I21 RX001757
6 · The paper itself

Abstract

Osteoarthritis (OA) is a chronic progressive, painful disease of synovial joints, characterized by cartilage degradation, subchondral bone remodeling, osteophyte formation, and synovitis. It is now widely appreciated that the innate immune system, and in particular Toll-like receptors (TLRs), contributes to pathological changes in OA joint tissues. Furthermore, it is now also increasingly recognized that TLR signaling plays a key role in initiating and maintaining pain. Here, we reviewed the literature of the past 5 years with a focus on how TLRs may contribute to joint damage and pain in OA. We discuss biological effects of specific damage-associated molecular patterns (DAMPs) which act as TLR ligands in vitro, including direct effects on pain-sensing neurons. We then discuss the phenotype of transgenic mice that target TLR pathways, and provide evidence for a complex balance between pro- and anti-inflammatory signaling pathways activated by OA DAMPs. Finally, we summarize clinical evidence implicating TLRs in OA pathogenesis, including polymorphisms and surrogate markers of disease activity. Our review of the literature led us to propose a model where multi-directional crosstalk between connective tissue cells (chondrocytes, fibroblasts), innate immune cells, and sensory neurons in the affected joint may promote OA pathology and pain.

Indexed as

Disease SusceptibilityNeuroimmunomodulationAlarminsAnimalsBiomarkersChronic PainDisease ProgressionHumansMiceOsteoarthritisSignal TransductionToll-Like ReceptorsAlarminsBiomarkersToll-Like ReceptorsAlarminsDAMPsInnate immunityOsteoarthritisPainTLR

Identifiers

PMID31612243
PMCPMC6858588
OpenAlexW2980729841

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.