ReviewJournal of neuroinflammation2026
Nociceptor neurons shape antiviral immunity.
Review in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- γδ T Cell-Mediated Neuroimmune Interactions in Skin Inflammation and Allergy.Clinical reviews in allergy & immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nervous and immune systems cooperate to protect the host, yet the contribution of sensory neurons to antiviral immunity remains incompletely defined. Nociceptor neurons do more than relay pain: they detect viral products and inflammatory cues through pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs), and respond to mediators such as type I interferons (IFNs), tumor necrosis factor (TNF), and interleukin-1β (IL-1β). Upon activation, these fibres release neuropeptides and neurotransmitters, including calcitonin gene-related peptide (CGRP) and substance P (SP), while sympathetic catecholamines provide a parallel neural input that shapes vascular tone, leukocyte trafficking, and effector programmes across tissues. Viral infection can also engage neuro-glial circuits in sensory ganglia and, in some settings, spread directly to the central nervous system (CNS), as described for lymphocytic choriomeningitis virus (LCMV), herpes simplex virus (HSV), and selected influenza A virus (IAV) strains. Here, we synthesize evidence that nociceptors shape antiviral immunity in a context-dependent manner rather than exerting uniform control. Nav1.8⁺ afferents restrain excessive inflammation while supporting dendritic cell (DC) priming of CD8⁺ T cells during cutaneous HSV-1 infection; vagal TRPV1⁺ neurons, a subset of Nav1.8⁺ nociceptors, promote disease tolerance during influenza by tuning lung myeloid responses; CGRP signaling drives T helper (Th) 1 differentiation during acute LCMV infection; and sympathetic adrenergic inputs deepen CD8⁺ T cell exhaustion during chronic infection. Defining these neuro-immune circuits may reveal therapeutic opportunities, but species differences, circuit heterogeneity, and the pleiotropic effects of shared mediators will need to be resolved before these insights can be translated to human disease.
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Registered trials
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 Socratic graph.