Inflammatory response in traumatic brain and spinal cord injury: The role of XCL 1‐XCR 1 axis and T cells
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Abstract Background Traumatic brain injury (TBI) and spinal cord injury (SCI) are acquired injuries to the central nervous system (CNS) caused by external forces that cause temporary or permanent sensory and motor impairments and the potential for long‐term disability or even death. These conditions currently lack effective treatments and impose substantial physical, social, and economic burdens on millions of people and families worldwide. TBI and SCI involve intricate pathological mechanisms, and the inflammatory response contributes significantly to secondary injury in TBI and SCI. It plays a crucial role in prolonging the post‐CNS trauma period and becomes a focal point for a potential therapeutic intervention. Previous research on the inflammatory response has traditionally concentrated on glial cells, such as astrocytes and microglia. However, increasing evidence highlights the crucial involvement of lymphocytes in the inflammatory response to CNS injury, particularly CD8+ T cells and NK cells, along with their downstream XCL1‐XCR1 axis. Objective This review aims to provide an overview of the role of the XCL1‐XCR1 axis and the T‐cell response in inflammation caused by TBI and SCI and identify potential targets for therapy. Methods We conducted a comprehensive search of PubMed and Web of Science using relevant keywords related to the XCL1‐XCR1 axis, T‐cell response, TBI, and SCI. Results This study examines the upstream and downstream pathways involved in inflammation caused by TBI and SCI, including interleukin‐15 (IL‐15), interleukin‐12 (IL‐12), CD8+ T cells, CD4+ T cells, NK cells, XCL1, XCR1+ dendritic cells, interferon‐gamma (IFN‐γ), helper T0 cells (Th0 cells), helper T1 cells (Th1 cells), and helper T17 cells (Th17 cells). We describe their proinflammatory effect in TBI and SCI. Conclusions The findings suggest that the XCL1‐XCR1 axis and the T‐cell response have great potential for preclinical investigations and treatments for TBI and SCI.
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Cellular mechanisms like apoptosis and autophagy may contribute to progressive hypothalamic-pituitary damage after TBI.
“Furthermore, cellular mechanisms like apoptosis and autophagy may contribute to progressive hypothalamic–pituitary damage [7,53,54].”
From Endocrine Dysfunctions After Pediatric Traumatic Brain Injury: Present Insights and Future Directions (2025) · cites this paper as [54]
The Pathophysiology of TBI section identifies apoptotic cell death as a mechanism of secondary injury, which can persist after TBI. It does not state that autophagy contributes to progressive hypothalamic–pituitary damage; a paper on apoptosis and autophagy in the HPA axis appears only in the References. (LLM, conf=0.86)
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The role of regulatory necrosis in traumatic brain injury
Nie, Z., Tan, L., Niu, J., & Wang, B. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.1005422 · Cited by 21 · see citing works
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Wang, J., Xu, L., Peng, D., Zhu, Y., Gu, Z., Yao, Y., Li, H., Cao, X., Fu, C., Zheng, M., et al. (2023) · Inflammation and Regeneration · doi:10.1186/s41232-023-00263-9 · Cited by 19 · see citing works
Inflammation drives fibrotic scars in the CNS
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Periodontal Disease Augments Cardiovascular Disease Risk Biomarkers in Rheumatoid Arthritis
Panezai, J., Ghaffar, A., Altamash, M., Åberg, M., Dyke, T. E. V., Larsson, A. O., & Engström, P. (2022) · Biomedicines · doi:10.3390/biomedicines10030714 · Cited by 18 · see citing works
Improved regeneration after femoral nerve injury in mice lacking functional T- and B-lymphocytes
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Interleukin-10 deficiency aggravates traumatic brain injury in male but not female mice
Gu, Y., Dong, Y., Wan, J., Ren, H., Koehler, R. C., & Wang, J. (2022) · Experimental Neurology · doi:10.1016/j.expneurol.2022.114125 · Cited by 16 · see citing works
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Research Progress on the Inflammatory Effects of Long Non-coding RNA in Traumatic Brain Injury
Wang, J., Li, C., Ding, W., Peng, G., Xiao, G., Chen, R., & Cheng, Q. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.835012 · Cited by 14 · see citing works
Zhang, Y., Chen, X., Fan, Y., Liu, J., & Li, Y. (2021) · The Nephron journals/Nephron journals · doi:10.1159/000518172 · Cited by 12 · see citing works
Linares, R., Gutiérrez, A., Márquez-Galera, Á., Caparrós, E., Aparicio, J. R., Madero, L., Payá, A., López‐Atalaya, J. P., & Francés, R. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.112653 · Cited by 12 · see citing works
The Natural History of Spinal Cord Injury
Haddad, A. F., Burke, J. F., & Dhall, S. S. (2021) · Neurosurgery Clinics of North America · doi:10.1016/j.nec.2021.03.003 · Cited by 8 · see citing works
Chemogenetic approaches to unravel circuit wiring and related behavior after spinal cord injury
Steenbergen, V. V., & Bareyre, F. M. (2021) · Experimental Neurology · doi:10.1016/j.expneurol.2021.113839 · Cited by 8 · see citing works
Dong, Y., Gu, Y., Lu, J., Wan, J., Jiang, S., Koehler, R. C., Wang, J., & Zhou, J. (2022) · Neurotrauma Reports · doi:10.1089/neur.2021.0064 · Cited by 8 · see citing works
Flagged first, then by citations
1 of the 109 references couldn’t be matched to a known paper.
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- Authors
- Zhang, M., Han, X., Yan, L., Fu, Y., Kou, H., Shang, C., Wang, J., Liu, H., Jiang, C., Wang, J., & Cheng, T.
- Affiliations
- First Affiliated Hospital of Zhengzhou University (CN)
- Zhengzhou University (CN)
- Corresponding author
- Jiang, Chao
- Wang, Jian
- Cheng, Tian
- Venue
- CNS Neuroscience & Therapeutics
- Publisher
- Wiley
- Published
- 2024-06
- Volume
- 30
- Issue
- 6
- Pages
- e14781-e14781
- ISSN
- 1755-5930 (ISSN-L)
- 1755-5949
- PMC
- PMC11183917
- OpenAlex
- W4399786795
- Cited by
- 32
- References
- 109
- Citations by year
- 2026: 17 · 2025: 12 · 2024: 3
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- CNS Neuroscience & Therapeutics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (82371339)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Keywords
- traumatic brain injury, spinal cord injury, T cell response, neuroinflammation, CD8+ T cells, natural killer cells, dendritic cells, IL-15, IL-12, interferon-gamma, Th1 cells, Th17 cells, secondary injury, inflammatory mediators
- MeSH terms
- Brain Injuries, Traumatic, Neuroinflammatory Diseases, Animals, Humans, Inflammation, Spinal Cord Injuries, T-Lymphocytes, Chemokines, C
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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