Evidence map›Paper›PMID 25446571›Full record

ReviewNeuropharmacology2015

The therapeutic potential of interleukin-10 in neuroimmune diseases.

A J Kwilasz, P M Grace, P Serbedzija, S F Maier, L R Watkins

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 4 pooled it
11.3field-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

133 citing papers in PubMed, 4 syntheses or guidelines pooled it, 222 citations in OpenAlex.

  1. Pooled it
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  12. Peripheral nerve injury reduces macrophage efferocytosis to facilitate neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  17. Hemp Hay (Animals : an open access journal from MDPI · 2025
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73 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

5 authors at 1 institution in 1 country.

A J KwilaszDepartment of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado-Boulder, Boulder, CO 80309-0345, USA. Electronic address: andrew.kwilasz@colorado.edu.
P M GraceDepartment of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado-Boulder, Boulder, CO 80309-0345, USA.
P SerbedzijaDepartment of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado-Boulder, Boulder, CO 80309-0345, USA.
S F MaierDepartment of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado-Boulder, Boulder, CO 80309-0345, USA.
L R WatkinsDepartment of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado-Boulder, Boulder, CO 80309-0345, USA.
University of Colorado Boulder · US

Funding

Preventing Transition of Acute-to-Chronic Neuropathic Pain: Models, Mechanisms &R01DE021966 · NIDCR · UNIVERSITY OF COLORADO · PI BARTH, DANIEL S., FLESHNER, MONIKA · 2011 to 2015
$2.0M
NIDCR NIH HHS R01 DE021966
6 · The paper itself

Abstract

Neuroimmune diseases have diverse symptoms and etiologies but all involve pathological inflammation that affects normal central nervous system signaling. Critically, many neuroimmune diseases also involve insufficient signaling/bioavailability of interleukin-10 (IL-10). IL-10 is a potent anti-inflammatory cytokine released by immune cells and glia, which drives the regulation of a variety of anti-inflammatory processes. This review will focus on the signaling pathways and function of IL-10, the current evidence for insufficiencies in IL-10 signaling/bioavailability in neuroimmune diseases, as well as the implications for IL-10-based therapies to treating such problems. We will review in detail four pathologies as examples of the common etiologies of such disease states, namely neuropathic pain (nerve trauma), osteoarthritis (peripheral inflammation), Parkinson's disease (neurodegeneration), and multiple sclerosis (autoimmune). A number of methods to increase IL-10 have been developed (e.g. protein administration, viral vectors, naked plasmid DNA, plasmid DNA packaged in polymers to enhance their uptake into target cells, and adenosine 2A agonists), which will also be discussed. In general, IL-10-based therapies have been effective at treating both the symptoms and pathology associated with various neuroimmune diseases, with more sophisticated gene therapy-based methods producing sustained therapeutic effects lasting for several months following a single injection. These exciting results have resulted in IL-10-targeted therapeutics being positioned for upcoming clinical trials for treating neuroimmune diseases, including neuropathic pain. Although further research is necessary to determine the full range of effects associated with IL-10-based therapy, evidence suggests IL-10 may be an invaluable target for the treatment of neuroimmune disease. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.

Indexed as

NeuroimmunomodulationSignal TransductionAnimalsDrug Delivery SystemsFemaleHumansInflammationInterleukin-10MaleMultiple SclerosisNeuralgiaOsteoarthritisParkinson DiseaseInterleukin-10Interleukin-10Interleukin-10 receptorMultiple sclerosisNeuropathic painOsteoarthritisParkinson's disease

Identifiers

PMID25446571
PMCPMC5144739
OpenAlexW1988768211

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.