Evidence map›Paper›PMID 36774519›Full record

ArticleJournal of neuroinflammation2023

Inducible co-stimulatory molecule (ICOS) alleviates paclitaxel-induced neuropathic pain via an IL-10-mediated mechanism in female mice.

Ishwarya Sankaranarayanan, Diana Tavares-Ferreira, Juliet M Mwirigi, Galo L Mejia, Michael D Burton, Theodore J Price

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 29 citations in OpenAlex.

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  8. Article
  9. GCN2 regulates paclitaxel-induced neuropathic pain.British journal of pharmacology · 2025
    Article
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  11. Article
  12. Review
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  19. Review
  20. Regulatory T cell-derived enkephalin gates nociception.bioRxiv : the preprint server for biology · 2024
    Article
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

6 authors at 1 institution in 1 country.

Ishwarya SankaranarayananPain Neurobiology Research Group, University of Texas at Dallas, 800 W Campbell Rd, Richardson, TX, 75080, USA.
Diana Tavares-FerreiraPain Neurobiology Research Group, University of Texas at Dallas, 800 W Campbell Rd, Richardson, TX, 75080, USA.
Juliet M MwirigiPain Neurobiology Research Group, University of Texas at Dallas, 800 W Campbell Rd, Richardson, TX, 75080, USA.
Galo L MejiaPain Neurobiology Research Group, University of Texas at Dallas, 800 W Campbell Rd, Richardson, TX, 75080, USA.
Michael D BurtonNeuroimmunology and Behavior Laboratory, Department of Neuroscience, Center for Advanced Pain Studies, School of Behavioral and Brain Sciences, University of Texas at Dallas, Richardson, TX, USA.
Theodore J PricePain Neurobiology Research Group, University of Texas at Dallas, 800 W Campbell Rd, Richardson, TX, 75080, USA. Theodore.price@utdallas.edu.
The University of Texas at Dallas · US

Funding

Translation Control of Pain PlasticityR01NS065926 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI PRICE, THEODORE J. · 2010 to 2023
$5.7M
NINDS NIH HHS NS065926
6 · The paper itself

Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a primary dose-limiting side effect caused by antineoplastic agents, such as paclitaxel. A primary symptom of this neuropathy is pain. Currently, there are no effective treatments for CIPN, which can lead to long-term morbidity in cancer patients and survivors. Neuro-immune interactions occur in CIPN pain and have been implicated both in the development and progression of pain in CIPN and the resolution of pain in CIPN. We investigated the potential role of inducible co-stimulatory molecule (ICOS) in the resolution of CIPN pain-like behaviors in mice. ICOS is an immune checkpoint molecule that is expressed on the surface of activated T cells and promotes proliferation and differentiation of T cells. We found that intrathecal administration of ICOS agonist antibody (ICOSaa) alleviates mechanical hypersensitivity caused by paclitaxel and facilitates the resolution of mechanical hypersensitivity in female mice. Administration of ICOSaa reduced astrogliosis in the spinal cord and satellite cell gliosis in the DRG of mice previously treated with paclitaxel. Mechanistically, ICOSaa intrathecal treatment promoted mechanical hypersensitivity resolution by increasing interleukin 10 (IL-10) expression in the dorsal root ganglion. In line with these observations, blocking IL-10 receptor (IL-10R) activity occluded the effects of ICOSaa treatment on mechanical hypersensitivity in female mice. Suggesting a broader activity in neuropathic pain, ICOSaa also partially resolved mechanical hypersensitivity in the spared nerve injury (SNI) model. Our findings support a model wherein ICOSaa administration induces IL-10 expression to facilitate neuropathic pain relief in female mice. ICOSaa treatment is in clinical development for solid tumors and given our observation of T cells in the human DRG, ICOSaa therapy could be developed for combination chemotherapy-CIPN clinical trials.

Indexed as

HyperalgesiaInducible T-Cell Co-Stimulator ProteinInterleukin-10NeuralgiaAnimalsAntineoplastic AgentsFemaleGanglia, SpinalHumansMicePaclitaxelAntineoplastic AgentsIcos protein, mouseInducible T-Cell Co-Stimulator ProteinInterleukin-10PaclitaxelCIPNIL-10 cytokineInducible co-stimulatory moleculePainT cells

Identifiers

PMID36774519
PMCPMC9922469
OpenAlexW4320019103

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.