ArticleJournal of neuroinflammation2014
Chronic thoracic spinal cord injury impairs CD8+ T-cell function by up-regulating programmed cell death-1 expression.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
- Neuro-immune interactions in tumors, immune-related disorders, and infections.Signal transduction and targeted therapy · 2026Review
- Peripheral immunosuppressive and immunostimulatory signatures of severity and pain in spinal cord injury.Journal of neuroinflammation · 2026Article
- Disuse Bone Loss After Spinal Cord Injury: Scope and Challenges, Potential Mechanisms, Treatment, and Future Directions.Journal of the Endocrine Society · 2026Review
- Neuroimmune Mechanisms in Traumatic Brain Injury and Cancer: Parallel Courses or Existence in Different Orbits.Biomedicines · 2026Review
- Mitigating sTNF/TNFR1 activation on VGluT2+ spinal cord interneurons improves immune function after mid-thoracic spinal cord injury.bioRxiv : the preprint server for biology · 2024Article
- PD-L1/PD-1 pathway: a potential neuroimmune target for pain relief.Cell & bioscience · 2024Review
- Clinicopathological characteristics and prognostic factors in axial chondroblastomas: a retrospective analysis of 61 cases and comparison with extra-axial chondroblastomas.World journal of surgical oncology · 2023Article
- Patients with Chronic Spinal Cord Injury and a Long Period of Evolution Exhibit an Altered Cytokine Production by CD4 and CD8 T Cell Populations.International journal of molecular sciences · 2023Article
- Clinicopathological and Prognostic Characteristics in Spinal Chondroblastomas: A Pooled Analysis of Individual Patient Data From a Single Institute and 27 Studies.Global spine journal · 2023Article
- Proinflammatory and Immunomodulatory Gene and Protein Expression Patterns in Spinal Cord and Spleen Following Acute and Chronic High Thoracic Injury.Journal of inflammation research · 2023Article
- Consequences of spinal cord injury on the sympathetic nervous system.Frontiers in cellular neuroscience · 2023Review
- Biomarkers from Secondary Complications in Spinal Cord Injury.Current pharmacology reports · 2022Article
- Central nervous system injury-induced immune suppression.Neurosurgical focus · 2022Review
- Revealing Potential Spinal Cord Injury Biomarkers and Immune Cell Infiltration Characteristics in Mice.Frontiers in genetics · 2022Article
- CCR7-mediated T follicular helper cell differentiation is associated with the pathogenesis and immune microenvironment of spinal cord injury-induced immune deficiency syndrome.Frontiers in neuroscience · 2022Article
- Revisiting the immune landscape post spinal cord injury: More than black and white.Frontiers in aging neuroscience · 2022Review
- Peripheral Immune Dysfunction: A Problem of Central Importance after Spinal Cord Injury.Biology · 2021Review
- Emerging Role of PD-1 in the Central Nervous System and Brain Diseases.Neuroscience bulletin · 2021Review
- Programmed cell death in spinal cord injury pathogenesis and therapy.Cell proliferation · 2021Review
- Immuno-hematologic parameters following rodent spinal cord contusion are negatively influenced by high-fat diet consumption.Journal of neuroimmunology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic spinal cord injury (SCI) induces immune depression in patients, which contributes to their higher risk of developing infections. While defects in humoral immunity have been reported, complications in T-cell immunity during the chronic phase of SCI have not yet been explored.
methodsTo assess the impact of chronic SCI on peripheral T-cell number and function we used a mouse model of severe spinal cord contusion at thoracic level T9 and performed flow cytometry analysis on the spleen for T-cell markers along with intracellular cytokine staining. Furthermore we identified alterations in sympathetic activity in the spleen of chronic SCI mice by measuring splenic levels of tyrosine hydroxylase (TH) and norepinephrine (NE). To gain insight into the neurogenic mechanism leading to T-cell dysfunction we performed in vitro NE stimulation of T-cells followed by flow cytometry analysis for T-cell exhaustion marker.
resultsChronic SCI impaired both CD4+ and CD8+ T-cell cytokine production. The observed T-cell dysfunction correlated with increased expression of programmed cell death 1 (PD-1) exhaustion marker on these cells. Blocking PD-1 signaling in vitro restored the CD8+ T-cell functional defect. In addition, we showed that chronic SCI mice had higher levels of splenic NE, which contributed to the T-cell exhaustion phenotype, as PD-1 expression on both CD4+ and CD8+ T-cells was up-regulated following sustained exposure to NE in vitro.
conclusionsThese studies indicate that alteration of sympathetic activity following chronic SCI induces CD8+ T-cell exhaustion, which in turn impairs T-cell function and contributes to immune depression. Inhibition of the exhaustion pathway should be considered as a new therapeutic strategy for chronic SCI-induced immune depression.
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Registered trials
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