ArticleJournal of neuroinflammation2021
Recruitment of γδ T cells to the lesion via the CCL2/CCR2 signaling after spinal cord injury.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Identification of the IL-1β/miRNA-326 axis as a key regulator of ferroptosis in spinal cord injury.BMC neuroscience · 2026Article
- The immune dysregulation landscape and dynamic regulation of competing endogenous RNAs in spinal cord injury.Frontiers in immunology · 2026Article
- Identification and Verification of Mitochondria-Related Diagnostic Markers of Spinal Cord Injury by WGCNA and Machine Learning.Behavioural neurology · 2026Article
- Engineered CCR2 positive macrophages coordinate immunoregulation with neural regeneration and matrix remodeling after spinal cord injury.Theranostics · 2026Article
- Degenerating intervertebral discs in the streptozotocin-high-fat diet model of type 2 diabetes show extensive inflammation.Disease models & mechanisms · 2025Article
- IL-17 + γδT cell: a new target in hyperbaric oxygen treatment reducing spinal cord injury.Journal of translational medicine · 2025Article
- The transcriptome and secreted factors of the intervertebral discs in STZ-HFD Type 2 diabetic male mice reveal extensive inflammation.bioRxiv : the preprint server for biology · 2025Article
- F-box/LRR-repeat protein 12 reorchestrated microglia to inhibit scarring and achieve adult spinal cord injury repair.Signal transduction and targeted therapy · 2025Article
- Identifying pyroptosis- and inflammation-related genes in spinal cord injury based on bioinformatics analysis.Scientific reports · 2025Article
- Integrated bioinformatics analysis of the effects of chronic pain on patients with spinal cord injury.Frontiers in cellular neuroscience · 2025Article
- Mechanism analysis and intervention strategies of the inflammatory microenvironment in traumatic spinal cord injury.Frontiers in immunology · 2025Review
- Gut-Spinal Cord Axis in Spinal Cord Injury: Bidirectional Inflammatory Mechanisms and Microbiota-Targeted Therapeutic Strategies.Journal of inflammation research · 2025Review
- Identification of Ifitm1 as a Pivotal Gene in Mouse Spinal Cord Injury Using Comprehensive Machine Learning Algorithms.Mediators of inflammation · 2025Article
- Exploration of biomarkers associated with histone lactylation modification in spinal cord injury.Frontiers in genetics · 2025Article
- Characterization of the Expressions and m6A Methylation Modification Patterns of mRNAs and lncRNAs in a Spinal Cord Injury Rat Model.Molecular neurobiology · 2025Article
- CCL2 Knockdown Attenuates Inflammatory Response After Spinal Cord Injury Through the PI3K/Akt Signaling Pathway: Bioinformatics Analysis and Experimental Validation.Molecular neurobiology · 2024Article
- Assessing the role of T cells in response to retinal injury to uncover new therapeutic targets for the treatment of retinal degeneration.Journal of neuroinflammation · 2023Article
- Optimized CAR-T therapy based on spatiotemporal changes and chemotactic mechanisms of MDSCs induced by hypofractionated radiotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 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
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundImmune cell infiltration and neuroinflammation are heavily associated with spinal cord injury (SCI). C-C motif chemokine ligand 2/C-C chemokine receptor type 2 (CCL2/CCR2) axis has been identified as a critical role player during the invasion of immune cells to lesions in many diseases. γδ T cells, a subgroup of T cells, manage the course of inflammation response in various diseases; however, it remains unknown whether γδ T cells are recruited to injury site through CCL2/CCR2 signaling and exert the regulation effect on neuroinflammation after SCI.
methodsBasso Mouse Scale (BMS), regularity index, cadence, max contact area, and motor-evoked potential testing (MEP) were measured to determine the neurological function recovery after spinal cord injury. Nissl staining was performed to identify the number of surviving motor neurons at lesion epicenter. Immunofluorescence, Western blot, enzyme-linked immunosorbent assays (ELISA), and quantitative real-time polymerase chain reaction (QRT-PCR) also were employed to evaluate the expression of associated proteins and genes.
resultsIn this study, we demonstrated that TCRδ
conclusionsIn conclusion, γδ T cell recruitment to SCI site promotes inflammatory response and exacerbates neurological impairment. CCL2/CCR2 signaling is a vital recruitment mechanism of γδ T cells to the SCI site, and it may be taken as a novel therapeutic target for future SCI.
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