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 accessAbstract
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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Different immune cells mediate mechanical pain hypersensitivity in male and female mice
Sorge, R. E., Mapplebeck, J. C. S., Rosen, S., Beggs, S., Taves, S., Alexander, J. K., Martin, L. J., Austin, J.-S., Sotocinal, S. G., Chen, D., et al. (2015) · Nature Neuroscience · doi:10.1038/nn.4053 · Cited by 1,442
Pain regulation by non-neuronal cells and inflammation
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Qualitative sex differences in pain processing: emerging evidence of a biased literature
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Astrocytes in chronic pain and itch
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Neuropeptide substance P and the immune response
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Self-citation
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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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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