ArticleBMC neuroscience2015
T cell deficiency in spinal cord injury: altered locomotor recovery and whole-genome transcriptional analysis.
Article in BMC neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Astrocytic Sirt2-Mediated Delactylation Limits Blood-Spinal Cord Barrier Reconstruction after Spinal Cord Injury.Research (Washington, D.C.) · 2026Article
- Integrated bioinformatics analysis of the effects of chronic pain on patients with spinal cord injury.Frontiers in cellular neuroscience · 2025Article
- Construction of a Searchable Database for Gene Expression Changes in Spinal Cord Injury Experiments.Journal of neurotrauma · 2024Article
- Retention of Human iPSC-Derived or Primary Cells Following Xenotransplantation into Rat Immune-Privileged Sites.Bioengineering (Basel, Switzerland) · 2023Article
- Spinal cord injury: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Inflammation and immunomodulation in central nervous system injury - B cells as a novel therapeutic opportunity.Neurobiology of disease · 2023Review
- Modulating neuroinflammation through molecular, cellular and biomaterial-based approaches to treat spinal cord injury.Bioengineering & translational medicine · 2023Review
- Transcriptomic analysis reveals the immune response of human microglia to a soy protein and collagen hybrid bioscaffold.Heliyon · 2023Article
- Single cell profiling of CD45Journal of neuroinflammation · 2022Article
- Effects of biological sex mismatch on neural progenitor cell transplantation for spinal cord injury in mice.Nature communications · 2022Article
- Human induced pluripotent stem cells integrate, create synapses and extend long axons after spinal cord injury.Journal of cellular and molecular medicine · 2022Article
- Sexual Dimorphism in Lesion Size and Sensorimotor Responses Following Spinal Cord Injury.Frontiers in neurology · 2022Article
- Strategies for Oligodendrocyte and Myelin Repair in Traumatic CNS Injury.Frontiers in cellular neuroscience · 2020Review
- Human immune cells infiltrate the spinal cord and impair recovery after spinal cord injury in humanized mice.Scientific reports · 2019Article
- Persons with Chronic Spinal Cord Injury Have Decreased Natural Killer Cell and Increased Toll-Like Receptor/Inflammatory Gene Expression.Journal of neurotrauma · 2018Observational
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundT cells undergo autoimmunization following spinal cord injury (SCI) and play both protective and destructive roles during the recovery process. T cell-deficient athymic nude (AN) rats exhibit improved functional recovery when compared to immunocompetent Sprague-Dawley (SD) rats following spinal cord transection.
methodsIn the present study, we evaluated locomotor recovery in SD and AN rats following moderate spinal cord contusion. To explain variable locomotor outcome, we assessed whole-genome expression using RNA sequencing, in the acute (1 week post-injury) and chronic (8 weeks post-injury) phases of recovery.
resultsAthymic nude rats demonstrated greater locomotor function than SD rats only at 1 week post-injury, coinciding with peak T cell infiltration in immunocompetent rats. Genetic markers for T cells and helper T cells were acutely enriched in SD rats, while AN rats expressed genes for T(h)2 cells, cytotoxic T cells, NK cells, mast cells, IL-1a, and IL-6 at higher levels. Acute enrichment of cell death-related genes suggested that SD rats undergo secondary tissue damage from T cells. Additionally, SD rats exhibited increased acute expression of voltage-gated potassium (Kv) channel-related genes. However, AN rats demonstrated greater chronic expression of cell death-associated genes and less expression of axon-related genes. Immunostaining for macrophage markers revealed no T cell-dependent difference in the acute macrophage infiltrate.
conclusionsWe put forth a model in which T cells facilitate early tissue damage, demyelination, and Kv channel dysregulation in SD rats following contusion SCI. However, compensatory features of the immune response in AN rats cause delayed tissue death and limit long-term recovery. T cell inhibition combined with other neuroprotective treatment may thus be a promising therapeutic avenue.
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