Evidence map›Paper›PMID 42091790›Full record

ReviewClinical reviews in allergy & immunology2026

γδ T Cell-Mediated Neuroimmune Interactions in Skin Inflammation and Allergy.

Shixiong Peng, Tetsuya Honda

Abstract readReview
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In one paragraph

Review in Clinical reviews in allergy & immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Shixiong PengDepartment of Dermatology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Tetsuya HondaDepartment of Dermatology, Hamamatsu University School of Medicine, Hamamatsu, Japan. hontetsu@hama-med.ac.jp.ORCID http://orcid.org/0000-0003-2355-4869

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

γδ T cells represent a distinct subset of immune cells that play pivotal roles in maintaining cutaneous immune homeostasis and regulating inflammatory responses. Accumulating evidence has established neuro-immune interactions as critical modulators of skin inflammation and allergic reactions, with γδ T cells emerging as a key cellular link between the nervous and immune systems. This review summarizes recent advances in our understanding of how γδ T cells coordinate neuroimmune crosstalk in inflammatory and allergic skin diseases. γδ T cells are characterized by rapid effector responses and pronounced functional heterogeneity, enabling them to sense neuronal cues and, in turn, modulate sensory neuron activity. Through the production of cytokines such as IL-17, IL-22 and IL-3, γδ T cells influence neuronal excitability, neuropeptide release, and itch transmission, thereby shaping both inflammatory intensity and sensory outcomes. Conversely, subsets of γδ T cells express receptors for neurotransmitters, allowing them to directly respond to signals derived from sensory neurons. This bidirectional communication positions γδ T cells as critical regulators linking neural sensing to innate and adaptive immune responses in the skin. Furthermore, we discuss the current blind spots in γδ T cell-related neuro-immune research, as well as potential perspectives and future directions for the field. A deeper understanding of γδ T cell subset specialization, neuron-immune coupling specificity, and tissue-context-dependent regulation will be essential for translating these insights into precise interventions for inflammatory and allergic skin disorders.

Indexed as

DermatitisHypersensitivityNeuroimmunomodulationReceptors, Antigen, T-Cell, gamma-deltaSkinT-Lymphocyte SubsetsAnimalsCytokinesHumansInflammationCytokinesReceptors, Antigen, T-Cell, gamma-deltaMolecular mechanismNeuroimmune interactionsSkin allergySkin inflammationγδ T Cell

Identifiers

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Registered trials

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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.