Regulatory T cells promote sensory neuron growth and protect against neurotoxicity.

Jessica P Hayes, Sandra Fok, Renee Whan, Gary D Housley, Gila Moalem-Taylor

Abstract read

In one paragraph

Article in Neurobiology of pain (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

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1 · What the graph read from it

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2 · The registry

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Jessica P HayesTranslational Neuroscience Facility & Department of Physiology, University of New South Wales (UNSW), Sydney, New South Wales, NSW 2052, Australia.

Sandra FokKatharina Gaus Light Microscopy Facility, Mark Wainwright Analytical Centre, Division of Research and Enterprise, University of New South Wales (UNSW), Sydney, New South Wales, NSW 2052, Australia.

Renee WhanKatharina Gaus Light Microscopy Facility, Mark Wainwright Analytical Centre, Division of Research and Enterprise, University of New South Wales (UNSW), Sydney, New South Wales, NSW 2052, Australia.

Gary D HousleyTranslational Neuroscience Facility & Department of Physiology, University of New South Wales (UNSW), Sydney, New South Wales, NSW 2052, Australia.

Gila Moalem-TaylorTranslational Neuroscience Facility & Department of Physiology, University of New South Wales (UNSW), Sydney, New South Wales, NSW 2052, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory T cells (Tregs) maintain immune homeostasis and suppress inflammation, and emerging evidence indicates they also modulate neuronal function and regeneration. Dorsal root ganglion (DRG) sensory neurons transmit pain signals and are damaged by chemotherapeutic agents such as paclitaxel (PTX), leading to neuropathic pain. Although Tregs show therapeutic promise in neuropathic pain, the mechanisms of Treg-neuron interactions remain poorly defined. Using in vitro co-culture, we examined interactions between primary DRG neurons and Tregs and their effect on PTX-induced neurotoxicity. Live-cell imaging showed that activated Tregs enhanced neurite length and branching and preferentially localised to neuron/neurite-rich regions. Additionally, activated Tregs rescued PTX-induced inhibition of neurite outgrowth. Pharmacological blockade identified Treg-derived amphiregulin (AREG) as essential for neurite outgrowth, while both AREG and neuropeptide Y were required for Treg-mediated protection against PTX-induced neurotoxicity. These findings identify Tregs as direct promoters of sensory neuron growth and protection from PTX-induced neurotoxicity through specific molecular mediators, supporting their potential therapeutic relevance in peripheral neuropathic pain.

Indexed as

Chemotherapy-induced peripheral neuropathyDRG neuronsPaclitaxelTregs

Identifiers

PMID42519388

DOI10.1016/j.ynpai.2026.100224

PMCPMC13382340

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