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The DOI matches its Crossref record; 175 of the 175 references it cites were found in a registry or an index.

Pathological pain and the neuroimmune interface

Open access
Grace, Peter M., Hutchinson, Mark R., Maier, Steven F., Watkins, Linda R.·2014·Nature Reviews Immunology

Abstract

Reciprocal signalling between immunocompetent cells in the central nervous system (CNS) has emerged as a key phenomenon underpinning pathological and chronic pain mechanisms. Neuronal excitability can be powerfully enhanced both by classical neurotransmitters derived from neurons, and by immune mediators released from CNS-resident microglia and astrocytes, and from infiltrating cells such as T cells. In this Review, we discuss the current understanding of the contribution of central immune mechanisms to pathological pain, and how the heterogeneous immune functions of different cells in the CNS could be harnessed to develop new therapeutics for pain control. Given the prevalence of chronic pain and the incomplete efficacy of current drugs — which focus on suppressing aberrant neuronal activity — new strategies to manipulate neuroimmune pain transmission hold considerable promise.

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Crossref · 10.1038/nri3621

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Metadata

Authors
Grace, P. M., Hutchinson, M. R., Maier, S. F., & Watkins, L. R.
Venue
Nature Reviews Immunology
Published
2014-02-28
Volume
14
Issue
4
Pages
217-231
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2035605437
Cited by
932
References
175
FWCI
9.33
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Pathological pain and the neuroimmune interface. https://app.cochat.ai/papers/10.1038/nri3621
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Grace, P. M., Hutchinson, M. R., Maier, S. F., & Watkins, L. R. (2014). Pathological pain and the neuroimmune interface. Nature Reviews Immunology. https://doi.org/10.1038/nri3621

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.